Journal articles
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.
Cited literature [54 references]
https://hal-amu.archives-ouvertes.fr/hal-01764672
Contributor : Carine Dou Goarin <>
Submitted on : Monday, October 29, 2018 - 2:38:01 PM
Last modification on : Saturday, October 3, 2020 - 3:21:16 AM
Long-term archiving on: : Wednesday, January 30, 2019 - 3:44:15 PM
Contributor : Carine Dou Goarin <>
Submitted on : Monday, October 29, 2018 - 2:38:01 PM
Last modification on : Saturday, October 3, 2020 - 3:21:16 AM
Long-term archiving on: : Wednesday, January 30, 2019 - 3:44:15 PM
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