4.3 Article

RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis

Journal

JOURNAL OF NEUROIMMUNOLOGY
Volume 276, Issue 1-2, Pages 142-149

Publisher

ELSEVIER
DOI: 10.1016/j.jneuroim.2014.09.006

Keywords

Demyelinating disease; Autoimmune disease; T cell differentiation; Gain-of-function; Genetic association

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Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in ROR gamma t transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. ROR gamma t transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology. (C) 2014 Elsevier B.V. All rights reserved.

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