NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells.

The Journal of experimental medicine 2020 Aug 03

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NKG2D is a danger sensor expressed on different subsets of innate and adaptive lymphocytes. Despite its established role as a potent activator of the immune system, NKG2D-driven regulation of CD4+ T helper (Th) cell-mediated immunity remains unclear. In this study, we demonstrate that NKG2D modulates Th1 and proinflammatory T-bet+ Th17 cell effector functions in vitro and in vivo. In particular, NKG2D promotes higher production of proinflammatory cytokines by Th1 and T-bet+ Th17 cells and reinforces their transcription of type 1 signature genes, including Tbx21. Conditional deletion of NKG2D in T cells impairs the ability of antigen-specific CD4+ T cells to promote inflammation in vivo during antigen-induced arthritis and experimental autoimmune encephalomyelitis, indicating that NKG2D is an important target for the amelioration of Th1- and Th17-mediated chronic inflammatory diseases. © 2020 Babic et al.

Citation

Marina Babic, Christoforos Dimitropoulos, Quirin Hammer, Christina Stehle, Frederik Heinrich, Assel Sarsenbayeva, Almut Eisele, Pawel Durek, Mir-Farzin Mashreghi, Berislav Lisnic, Jacques Van Snick, Max Löhning, Simon Fillatreau, David R Withers, Nicola Gagliani, Samuel Huber, Richard A Flavell, Bojan Polic, Chiara Romagnani. NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells. The Journal of experimental medicine. 2020 Aug 03;217(8)