by Anuja Vaidya/Medill News Service
Mast cells that play a role in healing and protection against pathogens in the immune system may contribute to the severity of autoimmune diseases such as multiple sclerosis, Northwestern University researchers are finding.
Immunologist Maggie Walker is helping to explain the role of mast cells in autoimmune diseases. Walker is a Ph.D. candidate in the Brown Lab run by Melissa Brown, a principle investigator at Northwestern's Feinberg School of Medicine. They found that mast cells can increase the severity of autoimmune diseases such as multiple sclerosis.
Mast cells have granules inside them that are made up of protein and histamine. When these granules are released, they are supposed to help clear away threats to the body, said immunologist Craig Smuda. But if they are activated in abnormal situations – the case with autoimmune diseases – the same granules and the things that the mast cells secrete
exacerbate the inflammatory cycles that occur.
Walker discusses her lab's research and gets candid about the best and most challenging aspects of working in science.
Q. What are mast cells? And what are some examples of autoimmune diseases?
A. Mast cells are known most for their role in allergies. They release large amounts of histamine in allergic reactions but they are also a cell type that contributes to the pathogenesis of a mouse model of multiple sclerosis. We mostly focus on a model of MS. Other than multiple sclerosis, some examples of autoimmune diseases are Type 1 diabetes and rheumatoid arthritis.
Q. Could you explain what happens to your body in these diseases?
A. Normally your immune system will detect an invader such as bacteria or virus and tell other immune cells to attack it, kill it and clear the infection. What happens in autoimmune
disease is that those same mechanisms happen but the response is pointed towards a self- tissue or protein. Your immune cells are actually destroying your own tissues. So it’s sort of
a misdirected natural response. This is the downfall of having these highly complicated immune systems that can fight a lot of pathogens – sometimes they fight the wrong things.
Q. What have you found during the course of your research so far?
A. We found that mast cells may not necessarily cause disease but that they contribute to it. There are these inflammatory responses that are happening in your body during MS or in
the mouse models of MS. Mast cells release mediators that exacerbate those inflammatory cycles. So without mast cells you get a little bit of disease, but with them you get much
more severe disease. They are playing an additive role to the underlying mechanism that are kind of known already.
Q. How do you go about your research?
A. We induce disease in mice and then analyze what’s happening to the cells and the tissues during disease. This entails taking particular cell populations out of specific tissues
and analyzing them.
Q. Why are you interested in this kind of research and why did you join this lab?
A. My mom actually has MS and so that gave me the inspiration to follow this field. I also really liked immunology when I took it in grad school. And then I really like Melissa Brown,
my boss. So it was an easy decision to join once I met her.
Q. What will the results of your research mean for humans?
A. It would be awesome if we actually came up with an idea that was somehow translated into therapy. It is sort of a niche though. It’s a different cell type that people haven’t
focused on before. So the likelihood of that happening is probably pretty small. But you never know what idea will boom into something important.
Q. What is the best thing about being a scientist?
A. The days when your experiments work and you get data that no one else has ever seen or done. It’s something totally novel and you know that you did it – you thought of it and
carried it through. The other good thing is the travel.
Q. And what are the challenging things about being a scientist?
A. The frustrations with getting experiments to work properly and to repeat themselves.
There is a lot of human error. You can think you are doing the exact same thing twice but you can get two totally different answers.
Q. What does this mean in terms of what you do?
A. If you can look at what I’ve done, it’s more like a branching tree as opposed to a forward and backwards. This is because every time you do an experiment and you get the answer,
you have a multitude of ways to analyze it and then to decide to what your next step is.
Q. What is next for the field of immunology in general?
A. Immunology can only go as far as technology allows it. Immunology is notorious for having lots of paradigm shifts. Its not just new information coming to light but it’s that
ideas actually shift. So its really getting tools that are good enough to figure out what’s really going on.
Q. And for your lab in particular?
A. Just further defining specific mechanisms. You start with the whole disease, then move to specific tissues, then move to specific cells and so on. So you just get more specific as
you go. That’s the goal.
