2010 October 29 | Ryan M. O'Connell, Daniel Kahn, William S.J. Gibson, June L. Round, Rebecca L. Scholz, Aadel A. Chaudhuri, Melissa E. Kahn, Dinesh S. Rao, and David Baltimore
This study investigates the role of microRNA-155 (miR-155) in autoimmune inflammation. *Mir155*^−/−^ mice were found to be highly resistant to experimental autoimmune encephalomyelitis (EAE), a model of autoimmune inflammation. MiR-155 functions in hematopoietic cells to promote the development of inflammatory T cells, including T helper 17 (Th17) and Th1 cells. The major contribution of miR-155 to EAE was found to be intrinsic to CD4+ T cells, although it also required for optimal dendritic cell production of cytokines that promote Th17 cell formation. These findings suggest that miR-155 plays a crucial role in promoting T cell-dependent tissue inflammation and could be a promising therapeutic target for autoimmune disorders.This study investigates the role of microRNA-155 (miR-155) in autoimmune inflammation. *Mir155*^−/−^ mice were found to be highly resistant to experimental autoimmune encephalomyelitis (EAE), a model of autoimmune inflammation. MiR-155 functions in hematopoietic cells to promote the development of inflammatory T cells, including T helper 17 (Th17) and Th1 cells. The major contribution of miR-155 to EAE was found to be intrinsic to CD4+ T cells, although it also required for optimal dendritic cell production of cytokines that promote Th17 cell formation. These findings suggest that miR-155 plays a crucial role in promoting T cell-dependent tissue inflammation and could be a promising therapeutic target for autoimmune disorders.