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

Autori
Babic, Marina ; Dimitropoulos, Christoforos ; Hammer, Quirin ; Stehle, Christina ; Heinrich, Frederik ; Sarsenbayeva, Assel ; Eisele, Almut ; Durek, Pawel ; Mashreghi, Mir-Farzin ; Lisnic, Berislav ; Van Snick, Jacques ; Löhning, Max ; Fillatreau, Simon ; Withers, David R. ; Gagliani, Nicola ; Huber, Samuel ; Flavell, Richard A. ; Polic, Bojan ; Romagnani, Chiara

Izvornik
Journal of Experimental Medicine (0022-1007) 217 (2020), 8; 20190133., 0

Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni

Ključne riječi
Autoimmunity, Innate immunity and inflammation

Sažetak
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.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti

POVEZANOST RADA