MicroRNA-155 promotes autoimmune inflammation by enhancing inflammatory T cell development.
Immunity, 2010/10/29;33(4):607-19.
O'Connell RM[1], Kahn D, Gibson WS, Round JL, Scholz RL, Chaudhuri AA, Kahn ME, Rao DS, Baltimore D
Affiliations
PMID: 20888269DOI: 10.1016/j.immuni.2010.09.009
Impact factor: 43.474
Abstract
Mammalian noncoding microRNAs (miRNAs) are a class of gene regulators that have been linked to immune system function. Here, we have investigated the role of miR-155 during an autoimmune inflammatory disease. Consistent with a positive role for miR-155 in mediating inflammatory responses, Mir155(-/-) mice were highly resistant to experimental autoimmune encephalomyelitis (EAE). miR-155 functions in the hematopoietic compartment to promote the development of inflammatory T cells including the T helper 17 (Th17) cell and Th1 cell subsets. Furthermore, the major contribution of miR-155 to EAE was CD4(+) T cell intrinsic, whereas miR-155 was also required for optimum dendritic cell production of cytokines that promoted Th17 cell formation. Our study shows that one aspect of miR-155 function is the promotion of T cell-dependent tissue inflammation, suggesting that miR-155 might be a promising therapeutic target for the treatment of autoimmune disorders.
MeSH terms
Animals; CD4-Positive T-Lymphocytes; Cells, Cultured; Encephalomyelitis, Autoimmune, Experimental; Glycoproteins; Hypersensitivity, Delayed; Interferon-gamma; Interleukin-17; Mice; Mice, Inbred C57BL; MicroRNAs; Myelin-Oligodendrocyte Glycoprotein; Peptide Fragments
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