Upon activation, CD4+ T cells of the adaptive immune system differentiate in different subsets of effector T helper (Th) cells named Th1, Th2 and Th17 with specialized effector functions. Each subset of Th cells orchestrates a specific immune response dedicated to clear pathogens, but when dysregulated, can also lead to the development of autoimmune and allergic reactions. Recently, a subset of CD4+ T cells that produces IL-17 (Th17) has been implicated along with Th1 cells in the development of autoimmune diseases such as multiple sclerosis (MS) and inflammatory bowel disease (IBD). However, how Th17 cells induce autoimmune disease development remains largely unknown. The mechanisms that induce autoimmunity can also promote tumor immunity and therefore be beneficial in some cancer. The laboratory's research focuses on understanding how Th17 cells are generated and how they can mediate their pathogenic functions and contribute to tissue destruction during the course of autoimmune diseases such as MS. The overall goal of the Bettelli laboratory's research is also to study the pathways, which modulate Th17 cells and develop strategies to block or enhance their functions.
This work promises to yield new insights into the mechanisms governing the autoimmune attack process and the genesis of pathogenic T cells in autoimmune diseases such as MS and into Th17 cell biology and functions. This holds great potential for the therapeutic manipulation of specific lymphocyte responses in the context of cancer and autoimmunity.