| First Author | Babic M | Year | 2020 |
| Journal | J Exp Med | Volume | 217 |
| Issue | 8 | PubMed ID | 32453422 |
| Mgi Jnum | J:294935 | Mgi Id | MGI:6457894 |
| Doi | 10.1084/jem.20190133 | Citation | Babic M, et al. (2020) NK cell receptor NKG2D enforces proinflammatory features and pathogenicity of Th1 and Th17 cells. J Exp Med 217(8) |
| abstractText | 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. |
