Dan R. Littman: 2016 Vilcek Prize in Biomedical Science

Dan R. Littman: 2016 Vilcek Prize in Biomedical Science


Probably everybody has heard that there
are at least 10 times as many bacteria in our gut as total cells in our own bodies. We only know for a very small number of bacteria what they actually do. My name is Dan Littman, I’m a professor of molecular immunology at the NYU School of Medicine and also a Howard
Hughes Medical Institute investigator. I was born in Bucharest, which is the
capital of Romania. I remember when I was about 5 years old Sputnik going up into space, the idea of having humans explore other planets was something that made me very excited. When I applied to college, I applied to an aerospace engineering program, but within the first year I decided to change my major to biochemistry. I was just totally transfixed by the questions that were being asked about the immune system. I became fascinated by T lymphocytes, the kind of cell that I’ve worked on for my entire career. During my postdoctoral work, I was trying to identify the genes that define the so-called helper cells versus killer cells. The first gene I was able to isolate was CD8 and very shortly thereafter the gene for CD4. It seemed like so many different questions could now be explored. In 1985, I was offered a position at the University of California. It was in the midst of the AIDs epidemic and it was a time when there was absolutely no way of combating the disease. It became very clear early on that HIV primarily infects T-helper
cells… that brought up the possibility that CD4 might be a receptor for the virus and indeed we as well as other people found that CD4 is the receptor that binds itself to the virus. At the beginning of 1996,
all of us discovered a molecule called CCR5. It has led to drugs that can be used
as an anti-viral to treat AIDs patients. We also continued to pursue our interest in studying how T lymphocytes develop in the thymus. That eventually took us into the discovery of the RORgammaT molecule. and what came as a big surprise was that RORgammaT is required for the development of a very unique subset of T lymphocytes called T helper 17 cells that are very important both for protecting our body surfaces, but at the
same time these are cells it could turn against our own tissues and cause
autoimmune disease. RORgammaT became right away an obvious target for therapy for
psoriasis, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel diseases. Our work on autoimmunity has now been extended to identify molecules that work along with RORgammaT that can be exploited to treat various autoimmune diseases. What’s particularly exciting is that the field in general has recognized that the microbes that inhabit our gut can have influence on many different physiology processes. Some of these are carried out through the immune system, some of these may be carried out through the nervous system, or through various metabolic pathways. What’s very exciting
about this, is that it should be possible to manipulate them for beneficial
purposes. There will very likely be a whole new class of therapeutics that will exploit the microbiota. I see a very, very bright future given the tremendous technological advances that we have seen in the field of biomedical research during the last decade be they genomic approaches, approaches at imaging that allow us to really probe deeply into cells, to probe deeply into the human body. There’s an enormous amount of potential going forward for learning more about how to treat human disease by having a better basic understanding of immune cells.

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