NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells.
J Exp Med
; 217(8)2020 08 03.
Article
em En
| MEDLINE
| ID: mdl-32453422
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.
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Base de dados:
MEDLINE
Assunto principal:
Artrite Experimental
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Células Th1
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Encefalomielite Autoimune Experimental
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Subfamília K de Receptores Semelhantes a Lectina de Células NK
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Células Th17
Idioma:
En
Ano de publicação:
2020
Tipo de documento:
Article