Speakers: Vijay Kuchroo (Harvard Medical School), Dan Littman (NYU), Laurie Harrington (University of Alabama), Daniel Cua (Schering-Plough Biopharma)Presented by the Neuroimmunology Discussion Group
Reported by Alan Dove | Posted July 2, 2007
For years, immunologists thought that Th1 cells were primarily responsible for autoimmune conditions such as multiple sclerosis and inflammatory bowel disease. But when mouse geneticists knocked out the gene encoding interferon-γ, which is required for Th1 cell development, they discovered that mice lacking Th1 cells could still develop autoimmune disease. Subsequent work uncovered a previously unknown helper T cell lineage, dubbed Th17 cells, which researchers now hypothesize may be responsible for autoimmunity.
A March 22, 2007, meeting of the Academy's Neuroimmunology Discussion Group addressed the resulting question: Is autoimmunity caused by Th1 cells or Th17 cells? Researchers looked at the role of various cytokine signaling pathways—including TGF-β, IL-6, IL-23, interferon-γ, and IL-17—in defining the fates of T cells, and how pushing the cells to one T-cell type or another affected the appearance of disease in mouse models. Speakers also discussed evidence that the nuclear hormone receptor RORγt may sit at the base of both the Th17 and Treg pathways, serving as the decision point between inflammation and suppression.
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