T-bet-dependent NKp46<sup>+</sup> innate lymphoid cells regulate the onset of T<sub>H</sub>17-induced neuroinflammation.
Kwong, Brandon; Rua, Rejane; Gao, Yuanyuan; Flickinger, John; Wang, Yan; Kruhlak, Michael J; Zhu, Jinfang; Vivier, Eric; McGavern, Dorian B; Lazarevic, Vanja.
; 18(10): 1117-1127, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28805812
A Metabolic Switch for Th17 Pathogenicity.
CD5L/AIM Regulates Lipid Biosynthesis and Restrains Th17 Cell Pathogenicity.
Th17 cells at the crossroads of autoimmunity, inflammation, and atherosclerosis.
IL-17 metabolically reprograms activated fibroblastic reticular cells for proliferation and survival.
Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.
Melatonin Contributes to the Seasonality of Multiple Sclerosis Relapses.
A two-amino-acid substitution in the transcription factor RORÎ³t disrupts its function in T<sub>H</sub>17 differentiation but not in thymocyte development.
Trans-presentation of IL-6 by dendritic cells is required for the priming of pathogenic T<sub>H</sub>17 cells.
Single-Cell Genomics Unveils Critical Regulators of Th17 Cell Pathogenicity.
Signaling via the kinase p38α programs dendritic cells to drive TH17 differentiation and autoimmune inflammation.