Chuan Wu

TL;DR: It is found that the production of TGF-β3 by developing Th17 cells was dependent on IL-23, which together with IL-6 induced very pathogenic TH17 cells, which had a molecular signature that defined pathogenic effector TH 17 cells in autoimmune disease.

TL;DR: It is shown that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity.

TL;DR: This paper showed that high salt intake affects the gut microbiome in mice, particularly by depleting Lactobacillus murinus, and treatment of mice with L. murinus prevented salt-induced aggravation of actively induced experimental autoimmune encephalomyelitis and salt-sensitive hypertension by modulating T helper 17 (TH17) cells.

TL;DR: This study identifies and validates 39 regulatory factors, embeds them within a comprehensive temporal network and reveals its organizational principles; it also highlights novel drug targets for controlling TH17 cell differentiation.

TL;DR: In this article, the authors used single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or differentiated in vitro under either pathogenic or non-pathogenic polarization conditions.