Neuroinflammation abetted by ILCs

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Science  22 Sep 2017:
Vol. 357, Issue 6357, pp. 1251-1252
DOI: 10.1126/science.357.6357.1251-e

The transcription factor T-bet is critical for the establishment of immunopathology in mouse models of multiple sclerosis (MS). T-bet is known to intensify the inflammatory potential of T helper 17 (TH17) cells, which are central players in MS. However, Kwong et al. find that the activity of T-bet in T cells is insufficient for the development of disease. It turns out that T-bet–dependent NKp46+ innate lymphoid cells (ILCs) regulate the infiltration of TH17 cells into the central nervous system (CNS). The ILCs produce a cocktail of proinflammatory cytokines that induce various factors, which disrupt the blood-brain barrier and allow TH17 cells to migrate into the CNS parenchyma. Characterization of ILC subsets (ILC1 and ILC3) could lead to new treatments for neuroinflammation.

Nat. Immunol. 10.1038/ni.3816 (2017).

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