Cambridge and Boston, MA. Wed. March 6, 2013 New work from the Broad Institute's Klarman Cell Observatory, Brigham and Women's Hospital, Harvard University, MIT, and Yale University expands the understanding of how one type of immune cell known as a T helper 17 or Th17 cell develops, and how its growth influences the development of immune responses. By figuring out how these cells are "wired," the researchers make a surprising connection between autoimmunity and salt consumption, highlighting the interplay of genetics and environmental factors in disease susceptibility. The results of their work appear in three companion papers in Nature this week.
The researchers concentrated on T cells because of their important roles in clearing foreign pathogens and in various autoimmune diseases. "The question we wanted to pursue was: how does the highly pathogenic, pro-inflammatory T cell develop?" said Vijay Kuchroo, co-director of the Center for Infection and Immunity at Brigham and Women's Hospital's Biomedical Research Institute and a Broad associate member. Kuchroo is also a professor of neurology at Harvard Medical School. "Once we have a more nuanced understanding of the development of the pathogenic Th17 cells, we may be able to pursue ways to regulate them or their function."
The human immune system is in a state of delicate balance: too little activity leaves a person vulnerable to foreign invaders, but too much activity threatens to harm the body it ought to protect. When this delicate balance is broken, it can lead to autoimmune diseases. But little is known about the molecular circuitry that maintains or upsets such a fine equilibrium.
"We wanted to understand how the body gets the right kinds of immune cells in the right amount, and how it keeps those cells at the right activity level so that they are not too active but also not underactive," said Aviv Regev, a Broad Institute core member and an associate professor of b
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Broad Institute of MIT and Harvard