With Vincent Racaniello, Cindy Leifer, and Stephanie Langel
Episode 1: Some like it hot
Aired October 31, 2017
Transcribed by Kim Barker
Content on Immune ( is licensed under a Creative Commons Attribution 3.0 License.

VINCENT: From Microbe TV, this is Immune, Episode 1 recorded on October 23, 2017.
VINCENT: Hi everybody, I’m Vincent Racaniello, and you’re listening to the podcast about the body’s defenders against disease. Joining me today for this first episode, from Ithaca NY, Cynthia Leifer.
VINCENT: Welcome.
CINDY: Thank you. It’s a bit cloudy here in Ithaca and about 55 degrees, 13 Celsius, so it’s actually a quite beautiful week this week.
VINCENT: My daughter just went back to Ithaca yesterday.
CINDY: Yeah, the leaves are changing, it’s just gorgeous here.
VINCENT: Yeah. Also joining us from Wooster, Ohio: Stephanie Langel.
STEPH: Hey now! Dr. R and Dr. L. It’s great to be here. Very excited to start this podcast.
VINCENT: And that’s the immune team- at least for now.
STEPH: Right, the tri-fecta.
VINCENT: That’s very good. And we’re going to tell you a little bit about ourselves and what we hope to do with this podcast, which has been in the making for quite awhile, had to find the right team. And we’ll tell you all about that. Let’s start with Cindy- I can call you Cindy right?
CINDY: Absolutely, please do, yes.
VINCENT: And you’re at Cornell University in Ithaca, New York, and I met you there earlier this year right?
CINDY: That’s correct, yeah.
VINCENT: So as part of my visit, I met with faculty and I met with Cindy-
CINDY: And I actually asked you at that time, I said, “When are you going to do a podcast on immunology”?
VINCENT: Ah, I’d forgotten that.
CINDY: Yeah you said, “Funny you should ask”-
VINCENT: And I said “Do you wanna do it?” and initially you said “No, I’m too busy”. But at some point, I don’t remember when, you said “Let me think about it”, right?
CINDY: Yes, I did.
VINCENT: And you decided to do it, which is great.
CINDY: Yeah I think communicating science in a broader audience is just so critically important so I’m thrilled to be involved in this.
VINCENT: Tell us your history- where are you from originally?
CINDY: I’m from Baltimore Maryland.
CINDY: Yeah, and I grew up there, and I went to college at University of Maryland, go Terps.
VINCENT: Oh listen ASV is going to be in College Park next summer.
CINDY: Oh cool- it has changed so much since I was there so, there’ so many new buildings and lots of new exciting science going on there. But that’s when I had an opportunity to work in a research lab and that was all she wrote.
VINCENT: Well did you go there as a bio major or a science major?
CINDY: I did- I thought that I was gonna go to medical school. I think this is a common thing that a lot of people say, but I wasn’t so thrilled about the constant memorization and regurgitation when I started to think about why things happened and how things interact. And I got in the lab and realized that hey, that’s how you can answer that. I said that’s what I wanna do. And so, from there I went to graduate school um, at Weill Cornell Medical College in NYC, and I was there for a number of years, and it’s funny because I never visited Ithaca while I was there. I was die-hard NYC, and from there when I finished up my PhD, which I did with Carl Nathan, who is known for macrophages and tuberculosis and nitric oxide and some interesting things like that, I went down to the NIH, the National Institutes of Health, to their intramural research program where I followed my passion looking at innate immunity, which we’ll talk about. There’s lots of parts of our immune system that are pre-wired and ready to go and so I was interested in looking at receptors that were really important for recognizing infectious diseases. And so I did that work down at the NIH and was there for about five years, it was an amazing immunology community down there and I was so glad to have been involved with all that. And then I started interviewing for faculty positions and I came to Ithaca and I really liked it, I really liked the department and I’ve been there since. Since 2005.
VINCENT: I just saw something the other day-you know Cornell is building something on Roosevelt Island I think- is that right?
CINDY: Yes they are. We have a tech college there.
VINCENT: I saw a release about some initiative to try and improve communication between New York Cornell and Ithaca Cornell and I’m not sure how that’s gonna work because distance is really an impediment.
CINDY: Well it’s not that far, its 4 and a half hours which seems like a really long way if you’re in NYC and things are so close together, but we have a bus and we love our bus and it goes back and forth two times a day and it has wi-fi so everybody works on there. So there’s lots of ways to try and foster the interactions between the multiple campuses so now we have the Weill Cornell campus as well as the tech campus, the campus here, and actually there are satellite campuses around the world as well. And there’s a big initiative with some money behind it, which is good to try and get some collaborations going. We are currently writing a proposal to have a joint retreat with the immunologists down at Weill and see if we can foster some more interactions.
VINCENT: When I was arranging my seminar trip the assistant said, “We do have a bus you could take”. I said, “Nope”. I took that bus so many times as a college student, I said “No more, sorry”.
CINDY: Oh, but it’s a different bus, we have a specific Cornell bus it’s called the Cornell campus to campus bus.
VINCENT: Yeah I’m sure it’s great.
CINDY: It’s super fancy, it has drinks and snacks.
STEPH: I hear sarcasm in his voice.
VINCENT: I’m sure it’s great, but I took a public bus and it was horrible. I had booked a flight and I got to the airport and the flight was cancelled, so I got back in my car and I drove.
CINDY: Sometimes it’s even better to drive, you know. We do when I travel internationally I actually drive down to NYC and take a plane out of there. Because we have a great close airport 10 minutes away but you have to travel to an in-between airport to get to where you’re going.
VINCENT: Steph what were you going to say, I interrupted you.
STEPH: Oh no, you’re fine. So Dr. L, you’re at the college of veterinary medicine, is that correct?
CINDY: I am, correct.
STEPH: And so within that college what is the department that you hail from?
CINDY: So I am in the department of microbiology and immunology.
STEPH: Somebody was commenting, looking at my background and your background, we have a very strong vet med presence on this podcast, our vet med game is strong as they say.
CINDY: That’s awesome, one of the things that really drew me here was the opportunity to look at comparative immunology across animals. And I haven’t done as much of that as I could, but I’m getting into that. We’re doing some canine research and dabbling in some other things. We’ve done some bovine research in the past, so we try to broaden out from our human-centric immune research.

VINCENT: So could you summarize briefly your research interests now in your lab?
CINDY: Yeah so overall I’m really interested in how our body recognizes infections and induces inflammatory responses. And how sometimes those responses go wrong. So we’re really interested in a particular type of cell called a macrophage, which we’ll talk about, and these cells are all over the body and they’re really the first responders. They recognize microbial infection and initiate the immune responses. And they do this using a particular class of receptors called toll-like receptors, which are very interesting in and of themselves, because Toll came from Christiane Nüsslein-Volhard, who won the Nobel prize for describing the role of Toll in Drosophila. And the story goes that she was making mutants of Drosophila and looked through the microscope and went, “Toll!” Which is apparently some sort of exclamation so that’s how she originally named the gene in Drosophila. And in humans and other animals we have toll-like receptors that are important in initiating inflammatory responses. And so we’ve looked for a long time at how these receptors are regulated and we’re particularly interested in how some of these recognize nucleic acids. And you might know that as DNA and RNA. And these receptors recognize DNA and RNA, but that’s highly conserved in viruses, bacteria, humans. So we wanna know why and how we can regulate recognition of DNA and RNA through these receptors. Why don’t we all have autoimmune disease? Because if you trigger these receptors inappropriately you end up with autoimmunity. So we try to understand how these receptors are regulated at the molecular level and at the cellular level.
VINCENT: Great. This is all great for our podcast. Steph, where are you from?
STEPH: Yeah, I’m originally from North Canton, Ohio, not too far from where I’m at now. I did my undergrad at Ohio State. I was in the animal sciences department. It’s a part of the agricultural and life sciences side of campus at Ohio State, but I also did a minor in biology. So really, throughout undergrad I thought I wanted to go to vet school. I very much identified with becoming a veterinarian. That was something pretty consistent until I did a summer rotating in a ruminant nutrition lab, and for some of those who might not know, a ruminant actually has 4 stomachs. They have a huge capacity of microbes, protozoa, fungi, bacteria, phages, which aren’t talked about as much, but this just cacophony of different types of microorganisms. And it really was from that rotation and then continuing in his lab that I just became hooked. And I became quite conflicted, because I don’t know if you have experienced this where you really identify with doing something for so long and then it changes and you really have to kinda take a breath and be like ok, I need to explore this further. So, instead of going off to veterinary school I decided to get a Master’s. For me, that was a good way to bridge between figuring out if graduate school was something I really wanted, I know a lot of people don’t do a Master’s in between the undergrad and PhD, but I felt it was really good for me. I went to Virginia Tech and I worked in immunology, but specifically worked with colostrum. So colostrum is the first milk that any animal, mammal, gives for their young. And the purpose of that is nutritional, obviously, fats and carbohydrates to sustain life. But really interestingly, what I think is getting a lot more attention is the cells and antibodies and a whole host of other immune components in that colostrum. So what we did is we took the colostrum, we fed it to calves with or without white blood cells- I should back up- what did I say, calves- I did mean bovine babies, so this would be little baby calves birthed from their mothers- to really see in a large animal model how these leukocytes of colostrum interact in the body. And we take them out in vitro we look at them in plates and try to determine what their functions are and how they act. So from there, I just knew that graduate school was it, a PhD was what I wanted, and I had this very heavy background in large animal livestock. I had worked on a dairy farm for years up until going to college, so I wanted to really get into the mechanisms of immunology, but I loved the idea of using a large animal model instead of a mouse to learn how the immune system reacts with pathogens. Um, so from there from Virginia Tech I actually did come back to Ohio State and not just because it’s my home state but also because my advisor, Dr. Linda Saif, she is really known for using pigs and cattle, piglets and calves, as models for viruses, for human diseases. And we do that using what we kind of term “bubble pigs” and “bubble calves”, which are germ free large animal models. And mice have this as well, kind of these “germ free” conditions where you can introduce a virus and see how that animal responds. So that’s what brought me here. What really made me fascinated and just very happy to be here with this program and project, my current research, is focusing on what we term the gut-mammary secretory IgA axis. And that’s kind of a mouthful, but the parts of that kind of explain what it is. So what I study is a porcine coronavirus that infects a pregnant mother then it infects through the gut, so it is an enteric virus. In the gut there are tons of lymph nodes and immune sites that have the capacity to generate B memory cells and plasma cells that secrete antibodies. And those antibodies, those plasma cells, are gonna come out of the gut, go into blood, and then circulate through blood, and we see, starting really in the third trimester in pigs and humans as well and mice, these cells start to be retained by the mammary gland. And they’re doing that because eventually they have to be secreted into milk to give the baby. So there’s this translational imprinting happening from what the mother’s infected or vaccinated with- the memory cells communicate to the baby through the milk. That process is what I’m studying and it’s really, I’m enjoying it a lot. Of course I have to work with very large pregnant pigs who do not like that I am manipulating their mammary glands as you can imagine, that wouldn’t be a fun time for anyone.
CINDY: Yeah pigs are temperamental.
STEPH: Oh they are. I’ve worked with a lot of large animals and I have to say if I’m to do a post doc in mouse models, which I hope to, I won’t miss milking 500 pound animals at 3 am. That’s for sure.
VINCENT: Wow that’s quite an experience.
STEPH: Yeah it is. It’s great, this program has led me to get some mechanistic type of research but also working in an applicable sense because this is relevant to farmers who do use pigs, and this virus is highly economically important. So I really hope to bridge this research, so we don’t know a lot about pregnant women immunology. We really have very limited vaccines for pregnant women, there’s only two that are FDA approved, and there’s really only four that people or groups are working on. So I would love to really use this experience to find ways to develop vaccines for pregnant women that enhance the life of them and their babies as well.
VINCENT: So you’re a PhD student. Do you know when you’re finishing?
STEPH: I am! Sometime next year, that’s always the question that I think I have heard from every family member and colleague who’s not in grad school. I don’t know if you all experienced that.
CINDY: Absolutely.
STEPH: So that just makes me sweat.
CINDY: I always said, “I’m done when I’m done you’ll know when I tell you”.
STEPH: Oh that is the perfect response. I think for this year I’m gonna post a status to family: don’t ask me at Christmas. No it’s sometime next year. I have a committee meeting coming up in January and we’ll review. Done a lot of pigs, a lot of experiments, so I’m hoping sometime next year, just not quite sure when. I have pigs right now so they better behave themselves, that will help determine when that date is.
VINCENT: So you said you’re going to do a post doc and then what’s your ultimate trajectory, what do you wanna do with your career?
STEPH: Yes, yes. Well I’d love to do a post doc. I’d really love to do one kind of culminating my experiences and do it in a lab that looks at mouse models and thinking about human diseases, and I’d really love to end up doing what you both do, having a lab focusing on immunology during pregnancy and the neonatal period and trying to develop vaccines that take advantage of the very special nature of a pregnant immune system.
VINCENT: Well, we’ll be interested to follow your career here on Immune.
STEPH: Thank you, I know, I was thinking about that. It’s a good thing, but also can be a bit you know, I feel my cortisol raising as I think about people who will listen.
VINCENT: Yeah, you’re making your career very very public, that’s true, and if you’d rather not talk about it that’s fine. When I started TwiEvo, This Week in Evolution, with Nels Elde, he had been at his assistant professor position for a few years and I said, “Let’s talk about the progress to tenure”, and so periodically he’d give us updates, and at one point he was up for tenure and waiting, and then he got tenure just a few months ago.
CINDY: That’s very fabulous.
VINCENT: And the cool thing was he was looking at other jobs in the meantime just in case and traveling all over and so forth so I think that’s cool, because it illustrated some of the things we have to do in this field, and people typically don’t know. So I think this podcast will be long lived and I hope that we can learn about what’s happening with your very young career. And by the way Steph, you’ve always called me Dr. R, and I think you should call me Vincent.
CINDY: Me too, call me Cindy.
STEPH: Ok- that’s fine!
VINCENT: And here’s the reason: I’ve been reading a book by Jon Yewdell called Truth Wins, which is a free download, we’ll put a link for that in the show notes. Everything about Immune will be at, and I’m already encouraging you to send in your emails: Truth Wins is a book that Jon Yewdell, who both of you will agree is an immunologist right?
STEPH: Absolutely.
CINDY: mmhmm
VINCENT: He’s written a book based on his career. He’s given a summary of what he did and how to be a biomedical scientist. It is just great because, for me, where my career is in its twilight, I love it cause I’m reading and going, “Oh yeah, that’s why I did that!” And for someone new, Steph, you should read this for sure.
STEPH: I will, it’s on my list!

VINCENT: I know you’re busy but it goes quick and here’s a quote that’s relevant; he’s talking about his experience, he went to Princeton and worked in Arnie Levine’s lab, and he writes, “First he made me call him Arnie, not Dr. or Professor Levine. This was actually quite difficult at first. Not until decades later did I really understand why this is so important. If the PI is Dr. so-and-so and everyone else is Pam or Jim, this creates a barrier for intellectual discourse. In a good laboratory the work has to based simply on the best ideas, not the source of the ideas.” It’s perfect, it’s absolutely perfect.
CINDY: I totally agree.
VINCENT: You level the playing field, right? So my first technician, she would call me Dr. R, Dr. R, and I said, “No, you can’t do that, I want you to call me…”, and it was hard because its hard you know but eventually. And if you forget, we’ll correct you.
STEPH: I might slip but you can correct me.
VINCENT: But I bet you call your PI Dr. Saif right?
STEPH: Yes, yes. I think I probably- I’ll feel most comfortable going first name once the program, once you get done and you can look back as more of a colleague. But right now, you know I kind of feel comfortable with the whole hierarchy of trainee and trainer. But here it’s great, I’ll do that.
VINCENT: That’s fine. So what we’re doing here, we started this podcast, we think one is needed in the field of immunology. And of course I’ve got a lot of podcasts under my belt and been doing it for 9 years. And we have all of them at we have a virology one, microbiology, parasitism, evolution, and a few others. And I’ve always wanted to start an immunology one but had to find the right people. Steph appeared on TwiV 356, and I’ve gotten to know her over the years through Twitter and so forth. You actually had a podcast for awhile with a dairy farmer right?
STEPH: I did, I did yes. Yeah.
CINDY: What did you talk about?
STEPH: Well what we did is he’s a really, well, he’s very thoughtful. He’s a really- he’s very thoughtful he’s a well-educated guy and he’s really interested in the science of farming, because there’s actually quite a bit of science in agriculture. I mean, agricultural science is big, and big business too. So we hooked up and we just talked about a lot of the different things, soil biology, we talked about infectious diseases in animals, so we really loved it but it got too busy I think with his schedule and mine to make it work and I was searching to do something more podcast-like so this came about.
VINCENT: He used to write in to TwiV because he was very interested in viruses and microbiology. I got to know him as well and they sort of base- you based your podcast on the TwiV model-you would do a paper-
STEPH: We did, yep.
VINCENT: I thought it was very good and then it stopped and I said, “Steph do you wanna do an immunology podcast?” And that’s how you got involved in this so…I mean the exact format we’re still not sure of. We’re gonna do papers of course, but we’d also like to mix it up a bit and maybe sometimes not do a paper and do things that are in the news that you might like to hear about. Today we’ll do a paper for you but send us your ideas you know, if you have things you’d like to talk about we’d love to hear it.
CINDY: And I’d like to hear if there’s specific things like immunology terms or mechanisms or interactions that you wanna hear about as well, because immunology’s really its own language and it’s so different from everything else we study with the web of interacting cells. It can be daunting to people to start to try and understand and unpack what goes on in an immune response.
VINCENT: Cindy do you teach an immunology course?
CINDY: I do, I teach a lot! I teach our basic immunology course and that’s mostly undergraduates. It’s a 400 level course so they take it usually in their senior year, although there’s a couple ambitious juniors and an occasional sophomore who take it. I also teach our advanced immunology class and that’s directed at graduate students and primarily our immunology graduate students or graduate students in other fields that have projects that use immunology really heavily and wanna understand it will take that course. And occasionally we’ll have a very ambitious undergraduate take that one. And then, I also teach veterinary students. So in veterinary school they have to learn immunology and we have a really intensive course where they actually learn all the -ologies: virology, parasitology, microbiology, epidemiology, and immunology all in the same course but-
Steph: Oh my gosh.
CINDY: But it’s really cool because they get to put it all together you know? They have these tutor sessions where they discuss cases, you know, where an animal comes in with x y z disease and they have to unpack that and they cross all those disciplines and use all of that information to synthesize them together to really learn in a deep way, and that’s fun to see. It’s really interesting to teach at all these different levels, and everyone has a different thing that they wanna get out of what they’re learning about immunology, so it’s fun.
VINCENT: Over on TwiV, what we did in the very beginning, we would do a series called Virology 101. And every few months we would just take an episode and do a basically, you know, introductory part. We would all talk, it was very different from a traditional lecture, but we would have slides and we would post those. We might think about doing that.
STEPH: That would be neat.
VINCENT: An immunology 101 going through the various concepts or dedicating an episode to it, if we get asked a question and so forth.
CINDY: I think it would be a great idea because I watched those Virology 101s when I had to tutor the veterinary students and I said I don’t really know the virology at all. And so I went and watched those and I encouraged my students to watch them as well.
VINCENT: Alright.
STEPH: There was a couple sentiments on Twitter; I had asked what do people want, and they said they’d love an Immune 101 just to help out with the terminology.
VINCENT: Alright.
CINDY: Well we’ve picked an interesting paper to talk about today, and maybe you guys will interrupt and ask some more basic stuff so we can get some of that 101 across.
VINCENT: And one thing we’re trying to do here is limit this podcast to an hour.
VINCENT: So now Cindy we have about 20 minutes.
CINDY: We have a challenge.
VINCENT: So tell us about the paper you’ve picked.
CINDY: So I’ve picked a paper that is a mouthful, especially if you’re not that familiar with immunology. But it’s called “Thermoneutrality but not UCP1 deficiency suppresses monocyte mobilization into blood”. And the senior author on this is Gwen Randolph, and she is at Washington University in St. Louis and interestingly she was a post doc when I was a graduate student, so I knew her. And so I followed her career, and she’s really interested in these monocytes. So these monocytes are these blood innate immune cells that play a variety of different roles in many many different diseases. But one of the things they do is they go out into tissues and they differentiate, so they become a slightly different kind of cell called a macrophage, and those are the cells I mentioned when I was talking about my own work. So I’m interested in those macrophages. And this caught my eye because she presented this work at a recent conference; the Society for Leukocyte Biology conference, and I was fascinated by this. Because they basically put mice at 4 degrees Celsius, at 22 degrees Celsius, and at 32 degrees Celsius. And we don’t often think about that because our mouse facilities where we house our mice are at 22 degrees. And it turns out they’re at 22 degrees because that’s a comfortable temperature for a human, and it’s not the most pleasant comfortable temperature for a mouse. A mouse actually prefers 30 degrees. So putting them at 4 degrees is like us going into Antarctica or something. And so she was really interested in what that does to these monocytes. Because she’s interested in lymphocyte trafficking and monocyte trafficking in the lymph, which is the equivalent of blood but it carries all the immune cells around the body. And her post doc was setting up some experiments and housing these mice at different temperatures and said, “Why don’t we do this cool experiment and see if they get atherosclerosis?” Because there’s this idea that there’s a protective effect of being at warmer temperatures so they say that people near the equator have lower incidence of atherosclerosis and heart disease. So does this have anything to do with this? So they put these mice at different temperatures and they have to use a special kind of mouse, because mice don’t get atherosclerosis. So they use mice that are deficient in a protein called LDL, which is low density lipoprotein, and carries fats around the blood, and if you have too much fat in the blood these bind up all the fats and the macrophages that are in your blood vessels take them up and they eat them and get filled up with this fat and cholesterol and become really inflammatory and damage the blood vessels. And it turns out that heart disease is a really big problem. You might know it, so it’s the number one cause of death in the United States, and it’s estimated that 316 billion dollars a year in healthcare costs go to treating heart disease. So understanding exactly how all this is happening is important. And so they are also interested in the idea that fat is not fat- it’s not all the same. We have what’s called brown fat and white fat. And our white fat is the jiggly stuff that we think about when we think about having that extra weight on our bodies. But brown fat is completely different. So brown fat has a whole lot of energy producing mitochondria in each cell, but they also express a lot of this protein that’s in this title- this UCP1- and what that does is it short circuits the production of ATP and instead of making energy it makes heat. And so this is the heat producing part of the body. So if you have more brown fat you produce more heat and you have less body fat. So they’re looking at all these different connections between this idea that the mice shouldn’t be at 22 they should be at 30, you have this brown fat vs. white fat and this UCP1, so all these things were floating around in their heads, and they said, “So let’s just do some easy thing- let’s take these LDL deficient mice that get atherosclerosis if you feed them the McDonalds diet and see what happens.” And when they did this it was amazing, because the mice at 30 degrees got much less atherosclerosis-
VINCENT: Than the lower temperature-
CINDY: Than the lower temperature mice at 22 degrees. And there was also some really interesting things in their first figure; the mice at 4 degrees ate twice as much as the mice at the other temperatures, so they ate a lot more but they didn’t gain weight. They had all of this brown fat, and this brown fat just made lots of heat. And in fact, if you took the temperature of these mice, the mice at 4 degrees had the highest body temperature. And the mice at 30 degrees had the lowest body temperature.
VINCENT: So they’re eating to regulate their temperature, the low environmental temperature right?
CINDY: that’s right, they’re eating a lot more just to regulate their body temperature, ‘cause they’re not producing as much energy, which is interesting.
VINCENT: In the wild, mice certainly live at very low temperatures, especially in the winter and so forth.
CINDY: They can yeah, they can, exactly. And so they have this ability to short circuit and make body heat when they’re cold.
VINCENT: So this UCP1- is that important for coupling diet and thermoregulation?
CINDY: It is. So when you don’t need the extra heat you downregulate expression of this protein. So the mice at 30 degrees have basically no detectable UCP1, and the mice at 4 degrees have very high levels of this so they make this brown fat and create all this heat. So they’re asking: is there this connection between expression of this protein and development of atherosclerosis. And so the bottom line is that it’s really complex, because they found different reasons for why a mouse at 4 degrees or 30 degrees does or doesn’t have atherosclerosis. But basically, after the first few experiments at 4 degrees they decided that those mice are very very different; they have high cortisol levels, short life spans, and they’re just very different from the other two at 22 and 30. So they focused the majority of their studies on comparing mice at our normal facility temperature of 22 and the higher temperature, thermoneutrality, at 30.
STEPH: Yeah I did have a question about the 4 degree temperature settings. So they discontinued that basically because of what you said; there was an inability for them to kind of extrapolate, and they couldn’t remove the complexity of: they were stressed, they died sooner, so is that why they discontinued?
CINDY: They did, yeah.
STEPH: It seems interesting to keep the 4 degrees treatment group. I mean, there definitely was huge differences…but that does make sense if it was too complex.
CINDY: Yeah it really added a whole other layer of looking at how the stress hormones are affecting immune cells and things like that so they really focused their studies on 22 vs 30.
VINCENT: So the title says “Thermoneutrality but not UCP1 deficiency suppresses mobilization of monocytes” right?
CINDY: Right, right.
VINCENT: So can you explain that conclusion?
CINDY: Yeah, so what they were trying to do is: the monocytes are in the blood, and they come out into the tissues like I mentioned, and they will go into the blood vessels and then they eat up the excess lipids. And so one of the things they found was that when they had these mice at 30 degrees and they were protected, they actually didn’t have significantly higher [she may have meant lower] cholesterol or anything, so they were wondering then- how are they protected from disease? Actually, what I should say is: they [30 degree mice] had higher levels in triglycerides with no difference in cholesterol. One would think though that if you had high triglycerides, which is the fat in your blood, that you would have a higher propensity for atherosclerosis, but they were lower. So, they started looking at where monocytes were. And so monocytes come out of the bone marrow and then they circulate around in the blood, and they’ll go out into the tissue. And they did some really cool experiments, including some analysis where you label the mice with these tracers and put them in this machine and read where their cells are, which is really cool. But what they found was that the monocytes stayed in the bone marrow and didn’t circulate as efficiently in the blood when the mice were at 30 degrees. So what that means is that if you have fewer precursors floating around in the blood, there’s fewer that get out into the tissue. And they show that, so the mice that are at 30 degrees and have the high fat diet just have fewer macrophages in their blood vessels when they develop atherosclerosis, so they develop less atherosclerosis.
VINCENT: Do we understand why the macrophages don’t come out as much in the high temperature?
CINDY: So, um, they looked a little bit at expression of different cytokine and chemokine receptors. So chemokines are really important for trafficking immune cells, and so they’re signals where one set of cells secretes a chemokine and another set of cells expresses the chemokine receptor and they’ll respond to that and move to where the chemokine is produced. And there’s a little bit of difference in expression of these chemokines involved in trafficking cells from the bone marrow into the blood and from the blood into the tissues. And so they think that that might be part of the reason why those cells are retained in the bone marrow and not leaving the bone marrow.
VINCENT: Ok. Now UCP1- do we know what it does? Is it a regulator of transcription or is it something else?
CINDY: No, it’s a protein that’s expressed in the mitochondria. And what it does is it short circuits the production of ATP. So we have the ATP synthase machinery that will take the hydrogen differential across the membrane and use that to generate ATP and energy, and what they do is they short circuit that so it creates heat instead of energy.
VINCENT: I see, that’s really interesting.
CINDY: Yeah.
VINCENT: So they say, they have an interesting part in this paper, they have a box called “Novelty and Significance”.
VINCENT: They have what is known, and one is as you say the incidence of cardiovascular events increases in colder temperatures.
CINDY: That’s right. And I live in Ithaca so…
VINCENT: So the question is: have they done studies where they look at people in warm vs cold temperatures- I guess that would be temperate vs. tropical climates- and seen a difference in cardiovascular events?
CINDY: So people have done epidemiologic studies, and they suggest yes that there is a higher incidence at colder temperatures. But we know there’s a lot of factors that contribute to that right? Depending on where you live in the world you have a different diet, different exercise, different exposure to light, there’s just a lot of things that are different. But there’s some epidemiologic connections.
VINCENT: Yeah. I think if you’re in the northeast of the US for example, which is cold in the winter, not only is it cold but it’s very stressful right to live here. You get stuck in traffic, and it’s hard to separate that as a complicating factor, whereas whenever I go to a warm temperature place I relax.
CINDY: That’s true, yeah, they showed the mice at 4 degrees were stressed. You know the other thing we have to keep in mind is they kept these mice at a steady temperature, so they kept these mice in a cold room, basically, at 4 degrees or they’re kept in the warm room. But we tend to be outside, inside, different temperatures, our internal offices and things are maintained at a relatively steady temperature. But we also put on jackets and clothes to maintain our temperature so it’s a little bit different than what these mice are experiencing, so that’s a caveat to these studies.
STEPH: It was interesting though that in that paper they did take a look- I think it was over 15,000 samples of people in the St. Louis, Missouri sample- they did the coordinates so you can look up probably the weather, and they did show that in the cold months they had the same trend of monocytes circulating. And so they would then extrapolate then to maybe that the same is being seen in bone marrow. But so I was thinking about brown and beige fat, and I just remember it’s been relatively recent that they’ve discovered that in humans. So how, what that means in a mouse compared to a human and how the mouse is using brown and beige fat differently than a human, I think that translation is gonna be important, especially since now we’re talking not just the movement of an immune cell but metabolism, glucose use, and comparing the two different species.
CINDY: That’s absolutely true. I mean, I think one of the key things here is what Gwen was telling me is they submitted this paper, and the paper came back, and they said, “What about humans?”, and that’s when they contacted this epidemiologist. And I was absolutely blown away they collected 1200 samples per month-a total of over 15,000 samples, and they just bled the people and measured their monocytes, and they could show a seasonal change, you know, a little bit subtle, but definitely a trend towards warmer months lesser monocytes in the blood and colder months more monocytes in the blood. So that was really interesting. And your point about this brown fat, it’s really an attractive target for weight loss, because people were thinking if we can trick the adipocytes, the fat cells, to be more brown-like and make heat instead of energy, we could be just like the mice when they have high levels of this going on; they have to eat more to maintain the same body temperature and energy level, so if we ate the same, theoretically, we should burn more energy and lose weight. And so that’s why there’s a lot of interest in this UCP1 and this brown fat and regulation of glucose metabolism in humans as a potential way to target obesity.
STEPH: I was also fascinated by how they talked about, you know, they were showing in previous studies that using cold or some type of cold snap with humans would promote glucose dispersal. And basically you said people might lose weight, but they really challenge that concept of well, OK, maybe the difference between energy metabolism and these monocyte dynamics are two very different things. And so kind of feeding off this idea that people should go into this extreme cold, I think about there are actually in like spas you can go into these like cryo- these big refrigerators because they’re trying-I don’t know exactly what they’re promoting, but I assume it’s somewhere along these lines that they’re trying to promote you lose weight. But this paper’s interesting, because they say, “Well hold on, because you could be promoting atherosclerosis if they already have high levels of fat and the triglycerides in their blood.”
CINDY: It’s true, because you know we think about, I think about it too, when you’re outside in the winter you burn more calories, right, because you’re colder, your body needs to produce more energy to maintain the body temperature. And so yes, one would think that if you go into one of those ice boxes, which I don’t think I wanna do that’s very unpleasant. But you know, theoretically you should burn more fat. But I think a key finding from this paper was that they’re measuring those cortisol levels. And so cortisol is that stress hormone, and those were through the roof, and I think, you know, the benefits that you might get of burning more energy are outweighed by the stress and the fact that when you have those high cortisol levels and stress it really does promote this higher level of fat in the blood and I think it’s gonna be counterproductive.
VINCENT: Mmm. So this provides insight into mechanisms, right?
CINDY: That’s right.
VINCENT: But most people don’t have a choice of where they live right? So you know, if you have to live in a cold weather area, what can you do to reduce cardiac events?
CINDY: You can uh eat less McDonald’s food, you can exercise, reduce your stress, don’t smoke, I think the American Heart Association has seven recommendations, and I don’t remember what they are; its diet, exercise, don’t smoke, um yeah and there’s a couple of other ones that are really important and those are gonna be the major mechanisms of reducing your risk of heart disease. I think going outside in the cold weather and diving into a snowbank in your underwear is probably not the best way to do it.
STEPH: And the opposite would not be true; don’t just think you can keep smoking and then move to Florida and you’ll be fine.
CINDY: That’s very true.
VINCENT: You know, with the increased global temperatures, eventually we’ll all be warm, who knows. You said mice don’t get atherosclerosis
CINDY: Right.
VINCENT: So even if you feed them very high fat diets they do not develop it?
CINDY: Not very much, not like a human. So in a human by the time you’re say a teenager you already have deposits in your blood vessels so that’s a scary thing and it just gets worse over time. And so the more you can do to try and follow those rules to lower your risk the better throughout life. But yeah, so mice they don’t get a lot of atherosclerosis unless you mutate the genes that are required for clearing the lipids from the blood. So the LDL mice, that’s the receptor deficient mice that I mentioned, so LDL receptor is on the liver cells and that binds to the low density lipoproteins that are in the blood and clears them. So you might know if you’ve ever gotten a cholesterol test, they measure HDL and LDL and the HDL is your good cholesterol and your LDL is your bad cholesterol. So the HDL is really good at clearing the cholesterol out of the body and the LDL is what builds up in the liver and is cleared by this LDL receptor, but if you lack that this LDL builds up in the blood vessel and causes atherosclerosis in the mouse.
VINCENT: Do we understand why mice don’t develop it? That would be good to know right?
CINDY: I don’t study atherosclerosis so I’m not sure if I fully understand why they don’t.
VINCENT: Yeah, it seems to me that if you could figure out the mechanism you might get insights into preventing it in people right? Besides diet and lifestyle changes.
CINDY: Yeah I think there’s a lot of people trying to understand that.

VINCENT: Lemme ask you a more basic question: A term used in this paper is monocyte and you work on macrophages. So what’s the difference, what are they?
CINDY: So they’re different versions of the same cell. So all the cells in the immune system derived from a hematopoietic stem cell in the bone marrow and they go through several rounds of differentiation into different blood cell types. And when this particular cell type, the monocyte, leaves the bone marrow, it circulates around in the blood and then it will exit the blood and enter the tissue and differentiate into a macrophage. And so it’s that tissue macrophage that’s doing the business end of what’s going on.
VINCENT: Yeah, and in different tissues they have different names, right?
CINDY: They do! So in the brain we call them microglial cells, in the liver we call them Kupffer cells, and there are osteoclasts in the bones. So they’re all derived from the same precursor. But there are some really interesting things that have come out in the last few years where tissue macrophages are actually two different populations. So one comes from these blood monocytes throughout life, but some of them are seeded during embryonic development from what’s called the yolk sac, which is on the liver in the fetus. So they exit very early during development and seed the tissues, and those are tissue resident macrophages, and they behave a little bit differently, although they can do the same types of things. But throughout life we’re constantly re-seeding the tissues with these blood-derived monocytes that differentiate into the macrophages.
VINCENT: And of course you talked about in this paper macrophages taking up lipids but they do many other things too right?
CINDY: Oh yeah, they’re phagocytes so they eat and they’re “macro” “phages” so they eat big things. And so they’ll eat bacteria, they’ll eat particles, they’ll eat lipids, basically anything you put in front of them.
VINCENT: And they’re also a kind of antigen presenting cell right?
CINDY: Yes, they do. And so antigen presentation is something we haven’t talked about, but there’s an important connection between pathogen infection and being able to produce antibodies that Steph was talking about. And so there’s this antigen presentation that has to happen in order for B cells, the antibody producing cells, as well as T cells, which is a cell type we haven’t talked about yet, but we need that antigen presentation to happen to activate those cells. So macrophages and another cell type called a dendritic cell are the key orchestrators. So they integrate the information from the microbe, they digest and present these antigens to the T cells and to the B cells indirectly and activate those components of the immune system.
VINCENT: And lest you think that monocytes are really awesome, they can be infected by viruses.
CINDY: They can yes.
VINCENT: Just about every cell can be right.
STEPH: I was thinking about that, and if they wanted to look at that in humans would they maybe see seasonality differences with viruses or bacteria? Because bacteria can infect monocytes as well and if you have an increase in the amount… I think I just was reading that Chikungunya in fact can actually infect monocytes and, well, that might be a bad example because typically that is in a warm weather climate, maybe you wouldn’t have the seasonality, but let’s just say another virus, would that virus be higher at the time monocytes are more prevalent in the blood? That would be really interesting to see.
CINDY: Well according to the seasonality of what they measured in the human samples, yes.
STEPH: Yeah.
CINDY: So during the colder times of year when we know influenza and some other viruses, not all, but some of the viruses circulate more, there’s more monocytes in the blood.
STEPH: Right.
VINCENT: That’s cool- that is a very cool study. By the way, it was in Circulation Research.
CINDY: Yes, and Gwen told me an interesting thing about the review process, so Circulation -they were looking for someplace to publish their study pretty fast, and Circulation Research claims they have an acceptance rate within 12 days.
STEPH: Oh my gosh!
CINDY: And so if you’re in this business and you know how long it takes to get a paper accepted, that sounds pretty good. Um now that’s obviously assuming that you can make edits in that amount of time, but I would think that the review would be done within that amount of time and then usually what happens is an investigator gets comments back from reviewers that say “Oh you didn’t do this you didn’t do that, what about this, think about that…” and then you revise your manuscript, do some more experiments and send it back. And in this case they did that whole human study, so I would imagine that they did not get it accepted in 12 days. But maybe they got the reviews back in that period of time and then it took them a couple of months to do the extra work before they resubmitted it again.
VINCENT: There are three co-first authors on this paper.
CINDY: There are.
VINCENT: Jesse W. Williams, Andrew Elvington, and Stoyan Ivanov
STEPH: This journal does a neat thing with those authors, I don’t know if you all had seen but they do little profiles…
STEPH: …of the first authors and they interview them.
CINDY: Yeah, so what Gwen told me is that the one, and I don’t remember if it was Andrew or Stoyan, started these studies, and he basically said, “Oh let’s put these mice in these different temperatures and do this really easy experiment”, and it turned out the striking phenotype. And so she was trying to get somebody to pick this up, and Jesse ended up picking this project up, and she said it wasn’t his main focus and so it took him a little while to get this project done, but it ended up being that he was first author on this. And in fact she told me he’s looking for a job right now, so he’s looking for his own lab if anyone’s interested.
VINCENT: Well he’ll get the Immune bump.
STEPH: Yes the Immune bump.
CINDY: Yes, whatever that’s worth, we’ll try.
VINCENT: Well we’re brand new so maybe right now not a lot.
STEPH: The bump will build over time.
CINDY: Maybe he’ll have a faculty position by the time.
VINCENT: Yeah, we always like to say people get the TwiV bump and so forth and we are… our goal with Immune is to make it in the same category, right, so you can get the Immune bump.
CINDY: Absolutely.
VINCENT: Um do we want to do picks of the week? Steph? On Immune?
STEPH: Yeah, why not I think we could. I don’t know if I actually have a pick- do you all have a pick?
VINCENT: Yeah well we did our homework, Steph.
STEPH: Oh I’m sorry I didn’t include mine!
VINCENT: Do you want to look for one while we give ours?
STEPH: Yeah sure, sure.
VINCENT: So that you- you don’t wanna be on Immune 1 without a pick Steph.
STEPH: No, I’ll find something.
VINCENT: Cindy what do you have as a pick?
CINDY: So I’m really fascinated and I picked this FDA approval of the second CAR T cell therapy. So this is a chimeric antigen receptor expressed on T cells, and the first one was approved a couple of months ago. That was Novartis that made a drug that they call Kymriah. And this second FDA approval is for Kite Pharmaceuticals, which Gilead just bought they must have known this was gonna happen for 12 billion dollars in August, so Kite has Yescarta I think is how you say it. But both of these therapies are this chimeric antigen receptor, and it’s a completely different way of manipulating the immune system. And without going into too much detail, what they do is take the patient’s own T cells out and then they express this chimeric antigen receptor that’s specific for a tumor, and its usually a lymphoid tumor so some sort of immune tumor like acute lymphoblastic leukemia or something like that, and so they manipulate the expression of a receptor on these T cells and then they put the T cells back into the patient and then the T cells go and attack the tumor and kill the tumor. And this apparently works really well when it works. It’s extremely dangerous to unleash that type of cell on the body and so there are a lot of side effects. And I think you covered this a little bit in TwiV; it’s an extremely expensive therapy. It’s a couple hundred thousand dollars for one patient, so I think its maybe not gonna be available for everyone. But it seems like it’s worked for pediatric patients and so it’s really a promising therapy.
VINCENT: Yeah we did do this on TwiV, a recent one, and its 475,000 dollars per treatment.
VINCENT: Because you know, it’s tailored to the patient, they have to take out your T cells and so forth and its expensive, which begs the question of who can actually get this right?
CINDY: Right, right.
VINCENT: Unless insurance companies are gonna pay for it, it seems like that would be an awful lot for them to pay for.
STEPH: Right.
CINDY: Yeah.
VINCENT: But that, I mean, it’s an interesting question; obviously, so I read some articles online in the Times where the developers of the drug said, “Well it’s worth it to save your life”.
CINDY: If you have the money it’s worth it…
VINCENT: Yeah that’s the thing, what if you don’t have the money?
STEPH: It’s kind of icky right to think that we’re putting emphasis on people’s lives based on the amount of money they have and I would hope insurance could cover it or with time- I mean I know they’re trying to recoup their costs of the billions of dollars that went into that but it’s a lot of money.
CINDY: It is a lot of money.
VINCENT: They can recoup their costs but the problem is they typically don’t lower the price after they’ve recouped their costs.
STEPH: That is the problem.
VINCENT: So a successful drug will then fund or fuel other programs in a company, so they don’t wanna lower the price. I think these are really really cool therapies.
CINDY: They are.
VINCENT: And Cindy, you should do the new one on Immune at some point, because I’d love to hear your view of it, you know ours was from a virological viewpoint because you deliver the CAR via a viral vector but…
CINDY: That’s right.
VINCENT: …but we’d love to hear others. And I love the name Kymriah, it’s kind of got chimera in it.
VINCENT: So there’s the thing, CAR, wherever I go now people are talking about CAR therapy.
VINCENT: And like if you don’t know what they’re talking about, what are you getting your car fixed or what? I was just at Tufts and they were talking about CAR and I was at Penn of course where the original CAR was developed and they just throw it around like- and that’s like you said Cindy, that’s immunology.
CINDY: That’s right. And to me, I think this gets at the heart of what I think this podcast is about and that’s explaining some of these new therapies and new immune-based approaches to people who don’t- who aren’t exposed to that. So what is a CAR T cell? What is a T cell? How does it work? And I think it would be great to go over that in a future podcast.
VINCENT: For sure. Yeah. We can do whatever we want. It’s limited by us really. I mean I guess our plan is to do once a month, but we may find that we wanna do more. But we’ll see.
CINDY: Well there’s certainly enough information out there to do weekly.
VINCENT: Oh yeah.
CINDY: You know, we’re all busy so we need to find the time to be able to do that.
VINCENT: Yeah. Alright, my pick is Truth Wins by Jon Yewdell, because everyone needs to read this even if you’re not a scientist you should read it to find out what becoming a biomedical research scientist is like. If you’re early stage like Steph you should read it because it’s got a lot of great tips. And even if you’re an old person like me and you’ve gone through it you should read it because it’s just neat to find his insights. I just love it, it’s just a really good book. Its free, I’ll put a link to the download in the show notes, and Jon is gonna be here in New York City in early November. Turns out his son is a scientist, I think he’s at Sloan Kettering in New York City. And they’re both gonna come to the studio and we’re gonna do a TwiV together.
CINDY: Oh that’s great yeah. He’s a character, he’s fantastic I really like him.
VINCENT: Yes, he’s quite the character, and you can tell by reading the book right?
CINDY: Oh yeah, he takes off the gloves and he really puts it out there.
VINCENT: Yeah it’s great I love it.
CINDY: It’s true and can be a little disheartening if you read that.
VINCENT: Yeah for sure.
CINDY: I liked his perspective on what it used to be like vs. what it is now because some of us are just experiencing what it is now and they don’t realize what science was like before, and you can get so caught up in the way papers are done now and the way science is done that sometimes we lose track of that truth, you know, that seeking the truth that he talks about and I think its really important. I love how he says “cutting the NIH budget is just stupid” because…
STEPH: Very to the point.
VINCENT: And you know it’s not just because we want to be paid, it’s because the return of biomedical science is huge! I always tell people your lives are great because of science and technology and I have a finance friend and she says, “No, it’s because of finance” and I said, “No, I’m sorry, you may give the money but you’d be dead if it weren’t for vaccines and medicines.”
CINDY: Yeah, right.
STEPH: Right and I’d argue also the way we produce food and the ability to produce a large quantity of food and our nutrition and the way we grow and develop based on modern agriculture can also be a little tip of the hat to biomedical, because of genetically modified organisms.
VINCENT: Totally. He tells a story about how after World War Two, the US realized the ability of the Allies to prevail was based on science; you know the radar, the sonar, the antibiotics, all this stuff. And a fellow named Vannevar Bush said to the president, “You need to invest heavily in the NIH”, and that’s where it all started really and we seem to be forgetting that today.
CINDY: We do.
VINCENT: You know, we’re forgetting basic research, meaning just do what you’re interested in and good things will happen as opposed to curing cancer right?
CINDY: That’s right.
STEPH: Right.
VINCENT: That’s what we call ‘translational’ and there’s a place for some of that, but you also need to let scientists follow their curiosity.
CINDY: And I think part of the problem is that the general public doesn’t understand what it takes and what we sacrifice and what we do, you know, with our passion to study this all the time with every ounce of energy and they just dismiss that.
VINCENT: Yeah and it’s too easy to say “Why are you working on worms and flies? What’s that gonna do?”‘
CINDY: That’s right.
VINCENT: Well you know what, it turns out it’s really relevant.
CINDY: It absolutely is, toll-like receptors were identified in flies.
VINCENT: So that’s what we try to do on these podcasts, and here’s another one for you to listen to. Steph, did you find a pick?
STEPH: I did, I had one the whole time I was just acting you know, just playing my role as the young PhD student.
VINCENT: Oh I’m glad I’m glad.
STEPH: No I actually did have something in my queue, a paper that I’m just starting to read and maybe readers would be kind of interested in doing it along with me, and we could even kind of touch upon it – I may do a little Twitter storm about how I read scientific papers as a PhD student, how I was taught. I may be able to kind of fulfil that role as the person who is still in the training process and maybe shed some light on how to go about tackling some of these papers. So this- it’s a recent paper. It recently was published just last week and it is in Nature Immunology. It’s kind of an intersection between TwiV and Immune, but I’m really fascinated with the idea of this hygiene hypothesis. Now, if you haven’t heard of it its really attributing the rise of asthma and allergy to the fact that we are not exposed to as many allergens and pathogens as maybe we once were when we lived in a less sanitary environment, we were more agrarian, um, and so they kind of contribute that the less amount of pathogens then your system cannot become tolerant to those over time, and then that results in a hyper-response to different allergens. So, what they did was they wanted to determine well if we take these infant mice and we give them a gammaherpesvirus, and can giving a young animal a virus affect the subsequent development of allergic asthma? And they determined that it did in fact, they used a house dust mite to induce the asthma after they gave the mice this murine herpesvirus 4, MUHV4, and they showed that the clinical observation of asthma was decreased. And they were able to look at the immune cells, and this really talks to some of the cells we were discussing today, with monocytes and macrophages, something that’s in these studies, and showed that the embryonic alveolar macrophages that are resident in the lungs with the infection of the herpesvirus, they were kind of moved out and replaced by monocytes with regulatory functions. So those regulatory functions were able to downgrade the response of the Th2 subset of helper T cells to the house dust mite. And I find this fascinating, I mean really you know the hygiene hypothesis has gone circles, people kind of dismiss it, it’s kind of old news, or people are really thinking this could be true. And, um, so so this paper is entitled “A gammaherpesvirus provides protection against allergic asthma by inducing the replacement of resident alveolar macrophages with regulatory monocytes”. So this is in my queue this week, this is a little night reading if anyone wants to read it with me; I don’t know, it doesn’t seem to be open access, we can lament that, but yeah I think it’s fascinating and we will talk about allergy and asthma and its relation to how people live in the environments that they grew up in and how what happened during your infancy can project the way you will respond to a variety of things in the future.
VINCENT: OK so can you put that link in the show notes for me Steph?
STEPH: Yeah sure can.
VINCENT: And maybe you’ll do it in the future right?
STEPH: Sure.
VINCENT: Cool. Alright, that’s Immune. This is Episode 1. It’ll be eventually on Apple podcasts. It’s at where you’ll find the show notes, which means links and references to things we talk about if you want to explore them further. And you should subscribe. I’m sure you all have a favorite podcast app that you use on your phone or tablet or computer, just subscribe so you get every episode as we release them. And as I said earlier, we’d love to get your questions, comments, suggestions: The scientists of Immune are Cindy Leifer from Cornell University- thanks Cindy!
CINDY: Absolutely, my pleasure.
VINCENT: Cindy is on Twitter, @CindyLeifer all one word.
CINDY: That’s right.
VINCENT: Steph Langel is at Ohio State University, thanks Steph!
STEPH: Thank you, this was wonderful.
VINCENT: @stephanielangel on Twitter. I’m Vincent Racaniello. You can find me at I’m @profvrr on Twitter. The music you hear on Immune is by Steve Neal. You can find more of his work at There’ll be a link in the show notes. Do you know this fella Steve Neal Steph?
STEPH: I do! Steve Neal, he’s actually my brother and he’s fantastic, and I just looked at that website, it does look like “Steven” Neal” all squished together but it’s just stevenealpercussion.
VINCENT: Steven EAL percussion right? Oh! Steve Neal. Right, sorry got it! So you can go see him, he’s got a performance schedule, look at this. Neat. So he’s a percussionist right?
STEPH: He is, he is. And he’s a lecturing professor at the College of Wooster so he does that too.
VINCENT: And so the music he wrote specifically for his sister, right?
STEPH: He did, he did.
VINCENT: How nice.
STEPH: Very very
VINCENT: Well thanks Steve. You’ve been listening to Immune, the podcast that’s infectious. Thanks for joining us, we’ll be back next month.