MicroRNA-155 promotes autoimmune inflammation by enhancing inflammatory T cell development

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, David Baltimore

Research output: Contribution to journalArticlepeer-review

696 Scopus citations

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.

Original languageEnglish
Pages (from-to)607-619
Number of pages13
JournalImmunity
Volume33
Issue number4
DOIs
StatePublished - Oct 29 2010

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