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T-bet-dependent NKp46(+) innate lymphoid cells regulate the onset of T(H)17-induced neuroinflammation

Abstract : The transcription factor T-bet has been associated with increased susceptibility to systemic and organ-specific autoimmunity, but the mechanism by which T-bet expression promotes neuroinflammation remains unknown. In this study, we demonstrate a cardinal role of T-bet-dependent NKp46(+) innate lymphoid cells (ILCs) in the initiation of CD4(+) T(H)17-mediated neuroinflammation. Loss of T-bet specifically in NKp46(+) ILCs profoundly impaired the ability of myelin-reactive T(H)17 cells to invade central nervous system (CNS) tissue and protected the mice from autoimmunity. T-bet-dependent NKp46(+) ILCs localized in the meninges and acted as chief coordinators of meningeal inflammation by inducing the expression of proinflammatory cytokines, chemokines and matrix metalloproteinases, which together facilitated T cell entry into CNS parenchyma. Our findings uncover a detrimental role of T-bet-dependent NKp46(+) ILCs in the development of CNS autoimmune disease.
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Brandon Kwong, Rejane Rua, Yuanyuan Gao, John Flickinger, Yan Wang, et al.. T-bet-dependent NKp46(+) innate lymphoid cells regulate the onset of T(H)17-induced neuroinflammation. Nature Immunology, Nature Publishing Group, 2017, 18 (10), pp.1117+. ⟨10.1038/ni.3816⟩. ⟨hal-01764672⟩

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