Demystifying MS: The Intersection Of Immunology And Neuroscience

Featuring Ann Herman, Senior Director and Senior Principal Scientist, OMNI-BD Inflammation and Infectious Disease, and Tracy Yuen, Senior Scientist and Biology Team Lead, Neuroscience.

Our understanding of what causes multiple sclerosis (MS) has transformed over the last few decades. While discoveries of the cell types involved in MS progression — both immune and brain — have led to major advancements for patients, there is still much to learn. Co-host Danielle Mandikian speaks to Ann Herman, Senior Director and Senior Principal Scientist, OMNI-BD Inflammation and Infectious Disease, and Tracy Yuen, Senior Scientist and Biology Team Lead, Neuroscience, to learn more about ongoing research that may inform future therapies.

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Transcript of Two Scientists Walk Into A Bar: “Demystifying MS: The Intersection Of Immunology And Neuroscience” with Ann Herman and Tracy Yuen

Maria: I’m Maria Wilson.

Danielle: I’m Danielle Mandikian.

Maria: And we are scientists. We. Love. Science.

Danielle: Yeah, we do. So, when we aren’t doing it, the next best thing is to talk about science! What’s really awesome is we are surrounded by some of the most brilliant minds in research!

Maria: So there is always someone interesting to talk to. But there’s never much time to just chat at work. That’s why we are so excited to be hosting this podcast. We are going to step away from the labs today to talk to other scientists about the cool stuff they are thinking about, working on and imagining...

Danielle: … as well as how some of these discoveries just might lead to new medicines. So, grab your favorite drink, get ready to unlock your science brain and join us for Two Scientists Walk into a Bar...

Maria: The show for scientists, science geeks and the people who love them!

Danielle: Hi, everyone, Danielle here and I'm stoked to get to talk about multiple sclerosis with two amazing scientists. Now I work primarily with cancer cells, but the pathogenesis of MS has always been interesting to me because it doesn't matter what disease you study, any time you're going to try to research and figure out how this disease gets to the quote unquote disease state, you start by looking at the endpoint and you have to work your way backwards. So, trying to figure out what all floodgates had to open in order to lead to that disease state can be very difficult to delineate. So today we have Ann Herman, an immunologist and expert on inflammatory diseases, and Tracy Yuen, a neuroscientist who studies the role of glia in neurological diseases and specifically the process of remyelination. More on that later... This is going to be fun!

Danielle: Welcome to the bar.

Ann: Thanks.

Tracy: Thank you.

Danielle: So before we get into multiple sclerosis, since we're all sitting here with masks on, I have to ask you both, how has COVID-19 impacted your research? Ann?

Ann: Yeah. I mean, obviously, everyone across the globe has had a major impact on, you know, their work life, and for us that's our research. But I think, really the first thing, coming from the MS space was just thinking about our patients and our physicians. Because, obviously, the immune system is very important for COVID. It's also involved in MS. And so, we set up a lot of collaborations with investigators across the globe, as well as looking in our own clinical trials. And we're really starting to be excited about the data that's coming out of that, and really being able to get answers to people on how this disease might affect them.

Danielle: How about you, Tracy?

Tracy: Yeah. I think an open question that, obviously, is emerging is that COVID clearly also affects the nervous system, too, and has lasting symptoms. And so, we don't really know what's going on there, but I think it’s kind of an open question that's being explored by the field. So, it will be interesting to see how -- you know, it's this interplay again between the immune system and the nervous system that's similar in MS, but also in COVID it's clearly playing a role, too. So, understanding the mechanisms, what's triggering it, etcetera, will be really interesting data to come, I think.

Danielle: Yeah, I agree, I think understanding the ins and outs of the virus will go a really long way to helping us understand why it affects so many different areas of the body. I also think that’s a good segue to talking about MS, right? So, let’s start with a general definition. Tracy, how would you describe MS from a neuroscience perspective?

Tracy: Yeah. So, in general, overall, MS is a demyelinating autoimmune disease. And it tends to affect younger patients, younger adult patients, so it's normally diagnosed between the ages of 20 and 40, which makes it especially detrimental because they start getting functional loss. And it's really initiated by immune cells infiltrating the brain and the spinal cord and damaging myelin. So, in terms of the neuroscience lens, we're really fixated and focused on the demyelination. So myelin in the brain and spinal cord is, basically, like insulation around a wire. And in MS and other diseases this myelin is lost and that causes demyelination, but also causes functional loss. So we're really focused on understanding how to regenerate that myelin, essentially.

Danielle: What about from an immunologist lens, Ann?

Ann: So, typically, it presents as what we call relapsing, or relapsing remitting MS, primary progressive MS, and then the patients with relapsing disease can also go on to progress and that's called secondary progressive MS. Now, we used to see these as really separate clinical presentations and even separate diseases almost. But recently, the role of inflammation has become really clear, you know, in some cases from how well some immunomodulatory therapies do in treating the disease. And that started us thinking that MS is really a continuum. So, the underlying biologies that cause relapse, or that cause progression are present across the course, but you might end up on the far end of the spectrum where you have more progression, or on the other side where you have more relapsing biology. And so, we really believe that, across the board the immune system is involved in all of these, which is a little bit different than years ago, when people thought that the progression was really just driven through purely neuronal degeneration. So, after the myelin is gone, as Tracy said, then the neurons break, or other processes happen. But it wasn't thought that immune cells were still involved. Now we know, you know, at the end of people's lives with progressive MS they'll have immune cells in the brain. And so, we do think that immune cells are involved throughout this disease continuum.

Danielle: So, what do we know about the demyelination process in terms of what triggers that to happen, versus what's the biology that drives it to fix itself when it does? Big question.

Tracy: Yeah, it's a pretty complicated question. Yeah. So, I mean in terms of the function of myelin and oligodendrocytes, right? I think for oligodendrocytes it's -- we're still learning so much -- they generate myelin. And as oligodendrocytes differentiate, it's pretty remarkable. They go from a precursor cell, this bipolar, simple precursor cell, to this super complicated cell with all these membranes, like super intricate morphology. It's actually over a 6,500-fold increase in membrane surface area, which is pretty crazy.

Danielle: That's massive.

Tracy: Yeah. So, it requires a lot of energy, a lot of nutrients, etcetera, oxygen. And the myelin sheath is actually really -- it's important. And oligodendrocytes are important for metabolic support to the axons just to function normally, for that kind of rapid conduction of nerve impulses. In terms of what triggers demyelination, that's sort of -- I mean, it's thought that immune cells, you know, traffic to the CNS and cause the demyelination. What triggers that is still really kind of unknown. And then in terms of remyelination, it's interesting because there is this age-dependent decline of that remyelination efficacy. So as people age, like most regenerative processes, it starts failing. And so is -- does remyelination in a disease like MS just start failing because of age? We don't know for sure. Right? It just -- we see a coincidental kind of progression that occurs with age. It's also just this interplay of glia. You have astrocytes, microglia, the vasculature that play a really important role in triggering and either supporting or, potentially, blocking and inhibiting remyelination. So, understanding that, obviously, is a huge can of worms, but important to understand for therapeutic potential. I don't -- my personal view, at least, is I don't think -- I mean, as much as we're interested in the remyelination biology, and as much as I think that there is promise there to address this progressive state of MS and kind of reverse, hopefully, that functional loss with remyelination, I don't think in isolation it will work for a disease like MS. Because it's still, at its core, heavily immune modulated. You know, having that component is really central for relief, addressing the disease overall. From the CNS space, at least I'll let Ann take the immune side of things. But there is in the remyelination space, even alone, there are kind of different schools of thought. So, for remyelination you're essentially trying to repair the insulation around a wire. If you think of an axon like a wire and the myelin sheath kind of like the insulation that allows for fast conduction of nerve impulses, we're trying to repair that damaged myelin to restore function. And it's both restoring function, but also nerve protection, as well. And people approach it in two different ways. There's either, basically, boosting intrinsic differentiation of the cells that myelinate, to then boost remyelination. And some people are also pursuing cell transplantation. So, there's different ways for approaching it.

Ann: On the immune side we're trying to stop the damage from continuing to happen. And, I mean, there's been immense progress made over the last 20 years in the MS space with multiple therapeutics available. And I think from the perspective of the immunologist, it's sort of one of big success stories. Because, you know, we didn't think that B cells were that important to the models that we work on. But when we got into humans, it actually turns out that they're very important. And we're still trying to figure out why. You know, it doesn't mean that other cells of the immune system aren't important, but there's something very central about what B cells do in the disease. And so, we've been able to modulate that. But, as Tracy mentioned, progression still happens. And what we're trying to get at really is that is there still some component of the immune system that we could target a therapy to or reduce more? And with that, you know, allow us to have even better benefits than some of the current drugs out there.

Tracy: And I think one of the open, more scientific questions also is just we don't even really fully understand how the immune system and how the central nervous system interact. Like even just a simple question like how B cells really interact with the CNS. We don't fully understand. So, I think there's a lot of science to be gleaned from a disease like MS because you can actually look at that interaction.

Wellington: Hey, Danielle!

Stephanie: Hi!

Danielle: Hey, guys! That's Wellington and Stephanie, my producers.

Wellington: Thanks for letting us interrupt! Couple of questions here. What is the CNS?

Danielle: Oh, yeah... acronyms. So CNS just stands for central nervous system, which is made up of the brain and the spinal cord. And within them there are many different types of cells like neurons and glia.

Stephanie: Okay, second question: glia. Are there different types of glial cells?

Danielle: Yeah, there are like some of what Tracy mentioned, there are oligodendrocytes and astrocytes. But as far as I understand, we're constantly in this process of really redefining and learning roles of cells. And a lot of these are defined by how they functionally support other neurons. So, I think there's also going to be room in the future for how we define these moving forward.

Danielle: From the immune cell side, what are the types of cells that you're seeing? I mean, because I know that, the way a B cell acts could have been look -- how it could be impacting whatever pathology. It could happen locally or in the periphery. So, what exactly are the key players that are infiltrating into those lesions that are in the brain?

Ann: Yeah. It's a great question. So, what we know is that many of the drugs that we give patients work peripherally. Right? So there is some impact you can have by blocking the cells from being activated or removing the cells from the system, you know, just from the peripheral immune system in general. But it's a much harder nut to crack to understand what's going on in the brain. So, there you have, you know, kind of your cells that have come in from the periphery, like B and T cells. You also have all these CNS-specific glial cells, we call them, which are kind of immune in nature. They are sort of like the brain's version of immune cells like macrophage or myeloid cells. And they're all playing a role in this very protected space. So those are a lot of the angles that we're kind of thinking about going forward; what other cells could we modulate, or are we just not getting rid of these adaptive B and T cells enough, you know?

Danielle: Uh-huh.

Tracy: And I think in the context of the CNS what makes it potentially more complicated is the resident immune cells in the CNS. Like microglia actually have a dual function, right? So, they can make things worse. They can exacerbate pathology and disease, but they also are really important for repair.

Danielle: Uh-huh.

Tracy: So, there's been a lot of work recently really looking at the beneficial side of inflammation, which is sort of flying in the face of conventional thought. But it's clear that they play a really important role, as well, there.

Danielle: I feel like every time I've even thought about immunology, just thinking about those different pathways and how it's not -- you can't really deem one as necessarily good or bad.

Ann: Uh-huh.

Tracy: Uh-huh.

Danielle: Like they always have to be balanced, always felt super-overwhelming.

Ann: Yeah.

Tracy: Yeah. And just therapeutic is what makes it hard. Right?

Danielle: Right. Yeah.

Ann: Yeah. There's definitely a yin/yang to the immune system. Do you know what I mean? Without the immune system you don't get wound repair. Right? And so, if the system is damaged, you need some types of immune cells and immune molecules to come in and repair it. And then vice versa. You know, we don't know why they start causing excess damage in the first place. So, it is really complex.

Wellington: Danielle, as a researcher, how do you think about this balance of treatment versus harming the natural system? How do you think about threading that needle?

Danielle: Yeah, my family always asked me this, and it's actually a huge focus in drug development. But the thing is that as we move towards treating more of these complex diseases where we're really focusing on cell-cell interactions, we have to do so with caution because in all honesty, we're still learning how these different systems actually interact with each other.

Danielle: Another kind of -- just since we're on this theme of like everything is really mucky -- [Laughter]. Okay, so here's my other question. You know how there's this big trend where people are always talking about personalized healthcare, and just kind of like looking at the way that this one person's disease is presenting, like what can you do that's unique to them to try to target their disease progression or existence of disease? Do you think that there would be any space for that perspective with MS? Just because like if you're having lesions in different places, and just depending on what exactly got pissed off in your immune system, is there any chance to try to hone in on that by patient-by-patient?

Tracy: Yeah. I mean, in terms of remyelination, like one of the things we're really fascinated with, and I think the field is also really fascinated with, is just this idea of heterogeneity. So, oligodendrocytes, you know, they're in the brain and the spinal cord, but ones in the brain versus ones in the spinal cord are actually quite different. They have intrinsically different properties. Which raises the question, do they actually have intrinsically different capacities to respond to different therapeutics? Right? So, getting at your heterogeneity question, lesions popping up in all these different areas, it's possible that if you have a lesion in your cortex versus your brainstem, maybe a different therapy would work better. But, I mean, very early days. I don't think we really have a sense for which one would be better. But it's definitely an interesting scientific question for sure.

Ann: That's really kind of the crux of what we try to ask. Our team is very focused on how could we identify patients who progress. You know, so can we understand who is going to get worse faster, and make sure that they're getting the therapeutics that they need earlier? And I think we're starting to get some traction on that, which is really exciting. But there's also other ways, you know, clinical presentation, age, demographics, etcetera, that we can already start to learn a little bit about this. And it's of broad interest across the field.

Danielle: So, we keep mentioning these lesions, but I don't honestly know exactly what they are. So, I don’t know, you guys are looking at each other. Ann -- [Laughs] -- what is this -- what are these lesions that we're talking about that are presenting on MRIs?

Ann: Yeah, so the classic lesions for MS are really what we call T1 weighted lesions on MRI. And they tend to light up with an enhancing agent like gadolinium. Which, basically, means that they're leaking. There's blood leaking into that lesion. And so classically in MS you when you diagnose somebody usually you find one or more of these. And you can either see the enhancing lesions, or you can see sort of the scars of those enhancing lesions. Then there is also a whole field of specialty imaging, which, you know, neither of us are expert in. That's really trying to look at progression and, specifically, slowly expanding lesions, or chronic evolving lesions, and lesions that have iron rims around them. So, there's a lot of new stuff in MS that we're using to sort of get a sense of progression beyond just looking at the patient's progression.

Danielle: Is that from like the blood-brain barrier being messed up, or it's just the?

Ann: Yeah. I mean, it's not quite as simple as a blood-brain barrier. But it's really like where the immune cells go in, and where they already have gotten in, they secrete a lot of things that inflame the vasculature. You know, it's kind of like when you get a splinter, and then all of the sudden you have this big red part. I mean, that's sort of the classic immune response is like heat, redness, swelling, edema. And, so that's essentially happening in the brain, and that's really what we see on the MRI lesions.

Danielle: So, Ann, you know, you talking about how everyone was surprised about the B cells being important for this process kind of reminds me of people thinking about immune responses for cancer. Is there a similar kind of backstory for that in MS?

Ann: Yeah. I mean definitely I think -- and knowing that story, as well, you know, it's like there's always someone in science who has an idea. And, they're very passionate about it, and they get a few people to follow them. But then the rest of the field is just like, "Oh, my gosh. Why does this person keep saying this idea over and over and over again?" And I would say for, you know, for MS that was Steve Hauser and his team at UCSF. Right? And so, he's kind of known as the grandfather of the B cell theory. And he, you know -- early on, I mean, we diagnosed MS through these things called oligoclonal bands, which are, basically, just antibodies. Right? So, it means that you have antibodies in your spinal fluid. And, of course, antibodies are produced by B cells. Right? And so that's sort of just a very basic nugget about why he thought B cells were important. But I think the power of that story is really that he never gave up. Right? And he, you know, convinced people to test this theory, even when the models weren't showing that B cells had anything to do with it. And, I don't know, you know, like when I was in grad school B cells -- studying B cells had kind of fallen out of favor. Right? So, we used to always joke as the immunology grad students: T cells are terrific and B cells are boring! [Laughter]. Now I've spent most of my career working on B cells because of people like Steve, who stuck to their guns and really found a way, kept pushing and proved that in humans B cells are really important for MS.

Danielle: So I guess are people looking at the existence of memory T cells for, I guess, whatever this immune response is?

Ann: For MS?

Danielle: Yeah.

Ann: Yeah. I mean, you know, I'm joking about B cells and T cells. But T cells are very important to the disease. We know that a lot of the genes that drive the susceptibility are expressed in T cells. We know that T cells are in the lesions and they're in the cerebral spinal fluid. So, I think it's really more, you know, it comes down to, from an applied science perspective, like how easy is it to modulate B cells versus T cells in a way that's safe for patients? Right? And we are doing research that shows that, when you modulate B cells, in general on a global level the T cells aren't affected at all, which we were kind of surprised about. But in actuality, when you look at the very specific B cell -- or T cells, excuse me, that are driving pathogenesis, those may be affected. And so maybe B cells just somehow have this special ability to when you remove them you lose these very specific MS T cells responses, but not the ability to respond with your T cells across the board, which is really great.

Danielle: So, I kind of feel like T cells are really having their time in the sun lately because in cancer research we're constantly trying to get T cells into the tumors and actually make them function once there. So everyone's really interested in this from multiple perspectives. So, Tracy, what cell are you most interested in?

Tracy: I would say I’m biased for oligodendrocytes. When Ann was talking about, kind of going against I guess convention, it was kind of funny, because I remember in grad school that was back when people thought glia did nothing. They just were glue supporting neuronal function. And I was like, "Why would you ever work on glia? They are the most boring cells. They just sit there." And now it's, you know, fast-forward quite a few years later, and we're realizing that not only are they central to development in disease, they actually can really drive a lot of the processes. But, yeah, I have a soft spot for oligodendrocytes because those are the ones that generate myelin. I think it's really also interesting to see that they don't just generate myelin. In my post-doc work we found that they actually induce angiogenesis during development, so they can have a lot of roles. I think we're only starting to understand now. And I think the field is moving very quickly to understand different subtypes of oligodendrocytes, how they're induced in disease during development, and also exploring -- I know this podcast is on MS, but like -- oligodendrocytes and glia in other diseases, they clearly play a lot of really central roles.

Danielle: So, did you get hooked on those cells early on? Or what kind of got you started on going after the quote unquote boring cells?

Tracy: I remember actually the exact experiment that got me really interested in glia. So as an undergrad I was looking at traumatic brain injury. And we had an in vitro model, where we would basically injure axons. And these cultures weren't pure, so we had other cells, glia, which at the time was like this other junk that stuck there. Right? And we were doing a lot of calcium imaging to look at different mechanisms and pathways of injury. And I noticed that all these other cells that were surrounding the axons basically lit up with the calcium dye before -- at lower levels of injury and temporally before the actual axon did. And so, at that point it was one of those things where we were like, "What the heck are these cells? What do they do? Why are they here? Why are they more sensitive to injury?" And so that just got me really interested. And then I switched over my grad school training and switched to oligodendrocytes and just fell in love because they're cool. [Laughter]

Danielle: I really love that. I mean, that's literally them giving you the red flag that they're more important than people think. Because of like lighting -- like literally lighting up and telling you.

Tracy: Yeah. That -- I mean, just, they're super-fascinating. And I also remember my grad school advisor -- you know, he's been studying oligodendrocytes for decades. And he would still run to the microscope and just stare at them in awe. Because they are beautiful. They have these beautiful processes. And I'm going to totally geek out. But, anyways, yeah. They're awesome cells.

Danielle: My PI was like that, too. I love working with other people that are that excited and happy.

Tracy: Yeah.

Danielle: What about you? What was your like going back to B cell -- the B side story?

Ann: You know, I think my original interest in science was just more actually on the personal side. When I was about 3 years old and my sister was 5, she got diagnosed with type 1 diabetes, which back in the day was, you know, really challenging to treat. And so, she would actually hide in the closet when my parents were supposed to give her injections of insulin. And so I think I happened upon her one time and was probably very loud like a 3-year old would be. And you know, so she pulled me in the closet with her and then we would hide in the closet. And we were just always so shocked that my parents could find us. [Laughter]

Danielle: ...way better at hiding.

Ann: Yeah. But I remember it in my little brain at that time. I didn't even know what a scientist was, but I was like, "I'm going to find something to fix my sister." And like that was my motivation. And, so going into science it was like I was almost nervous that I wouldn't like it, you know, because I had made this promise to my younger self. But, fortunately, I loved it. And I did work on type 1 diabetes for many years. And then MS is like the sister disease to type 1, where we always -- you know, if we're going to test something for type 1 diabetes we test it for MS and vice versa. So, I was very familiar with it, which I think is why I was sort of poised for the opportunity when it came up. And then it's just been amazing to feel like you really potentially are having impacts on patients' lives. Yeah.

Danielle: That's very sweet. I didn't realize that they were so close to each other.

Ann: Yeah. I mean, you know, they're both autoimmune diseases. In MS the immune system attacks the nerves, and in type 1 diabetes it attacks the beta cells that produce insulin. And, like we said earlier we still don't really know why, but we've learned a lot over the years. And even the genetics is almost -- is very overlapping between MS and type 1. So, yeah, I felt really enabled to just jump right into this field and kind of understand it. But then I've also been super lucky to have people like Tracy and other people and physicians that have been very patient to educate me about the neurology-specific side of things. So that's been super helpful.

Tracy: Yeah. I will say that's the fun part. Right? Because MS, like it can kind of -- it's two different types of science, immunology and neuroscience. And so, yeah, it's really fun working with people like Ann because you learn so much. And it forces you to think about your science in a totally different way. So, they bring everybody that we work with, you know, they bring different perspectives and it makes you refine your science and think about it more.

Wellington: Danielle, hang on, what is your favorite cell?

Danielle: Oh, all right, so keep this on the DL, but my favorite cell type is actually neurons, specifically principal neurons, because those are the ones that are kind of regulating communication between multiple cells. And I like to think of them as the bouncers of the information highway.

Danielle: So, then the natural question is, what do you foresee happening in your therapeutic space for treatment of MS? Like in the near future, versus far future. Or do you -- you know, the question that my family always likes to ask is like, "So are we going to see a treatment? Is this going to happen in our lifetime?" What do you think?

Tracy: Yeah, it's a tough question. I mean I tend to try to be optimistic. Right? So, the hope is that, you know, we've addressed the immune system component of MS pretty well. And now it's really tackling the progression aspect. And I will say the field has moved quite quickly in the last, you know, five, 10 years. We actually have compounds that boost remyelination that are being tested in the clinic, which is exciting. I think it leaves the big question of how to actually measure remyelination in the clinic, which people are trying to tackle. But I think the more data we get the better we'll get there. I mean, my hope is that we're at the point hopefully in my lifetime, this is the dream, that we can actually really keep MS under control for patients, and it’s not so much, you know, a devastating diagnosis for people. That's my hope, at least.

Danielle: That's really tough, though. Right? Because it's kind of like you can only rely on patients that are having a -- they've had enough damage to where you're actually seeing them have some kind of behavior or -- and I'm not -- I don't know if behavior is the right word, but like --

Tracy: Like functional --

Danielle: Yeah, some kind of functional problem, and then wait for them to be able to overcome it. I just -- I guess I hadn't thought about it like that.

Tracy: Yeah, that's a tricky part, too, because then it comes to this whole chicken or egg issue. Like you want to address it before it happens. And so, with Ann's group really trying to find a biomarker for that early progression would be critical. Because if you can then measure that, and then see that a therapeutic intervention helps with that, that's huge. And then, potentially, you could just stop all the functional decline from happening in theory. Right? So...

Danielle: Well, so same question to you, Ann. Like what, what do you foresee being kind of major events in the field like in the near-term versus long-term?

Ann: Yeah. Actually you guys set me up really, really well, because this is something I think about a lot and that we're actually trying to start now, is how could we diagnose someone before they even know they have MS? Right? So, in 20 years maybe you know your genetic background, you know maybe you have some genetic risk susceptibility for this disease. And then your physician once a year gives you a blood test, or even a finger stick test that tells you, "Oh, actually this year something is looking a little bit abnormal." And then you go off to have your MRI or have some other test that suggests you're in early progression. And there is a syndrome called Radiologically Isolated Syndrome, which is people who just happen to have an MRI for another reason, and then they show up with a lesion that looks exactly like an MS lesion. Those people are very likely to develop MS, but they don't yet have any clinical symptoms at all. So, if you could find people actively in that stage, treat them with something, maybe you could even just treat them once or for a year, and then prevent something from happening for five or 10 years. Or maybe -- I mean, cure is a big word in our field, but we would like to think about if you intervened early enough could you actually cure MS?

Tracy: I think that's the exciting thing that just the term is even being thrown around. Right? Because other diseases it's not even within the realm of possibility yet. So, I mean, even in just the last 20 or 30 years we went from having no therapeutics to, you know, a dozen or more therapies that actually work for some patients. So, that’s the hope, right?

Danielle: Great conversation. Thank you so much for joining us. And we're really looking forward to seeing what all comes out.

Ann: Yeah. Thank you. It was fun.

Tracy: Thanks for having us. That was fun!

Wellington: That was really cool. I love the underdog B-Cell story and I really, really like when you guys start talking about a cure because the word cure is not something that you scientists say that much.

Danielle: That is so true. And we also love being able to use the word cure, right? I mean, when we get up and we put our all into the research that we do every day, we're not trying to just treat symptoms. What we really want to do is stop the disease and cure it. And even more so Ann had been mentioning trying to figure out any kind of indication that someone might get sick so we can try to prevent them from even getting to that state like that's the ultimate dream.

So that's our show! Next time, Maria is going to look at what is happening around asthma, another very complex disease with surprisingly different mechanisms. And I can't wait for that. In the meantime, be sure to revisit your favorite episodes wherever you get your podcasts and make sure to subscribe if you haven't already. If you have any questions about MS or the science that we discussed today, go ahead and write to us. We're going to have a grab bag segment where we'll actually answer questions from listeners on a future show. Use our general email address [email protected]. That's G-E-N-E dot com.

And now for me, it's back to stalking cells!