Dendritic cell MST1 inhibits Th17 differentiation.

Authors:
Li C1,2, Bi Y3, Li Y1,2, Yang H2, Yu Q1, Wang J1,2, Wang Y1,2, Su H1,2, Jia A1, Hu Y1, Han L1, Zhang J1, Li S1, Tao W4, Liu G1,2
In:
Source: Nat Commun.
Publication Date: ()
Issue: :
Cells used in publication:
Dendritic cell (NHDC), human
Species: human
Tissue Origin: blood
Experiment


Abstract

Although the differentiation of CD4+T cells is widely studied, the mechanisms of antigen-presenting cell-dependent T-cell modulation are unclear. Here, we investigate the role of dendritic cell (DC)-dependent T-cell differentiation in autoimmune and antifungal inflammation and find that mammalian sterile 20-like kinase 1 (MST1) signalling from DCs negatively regulates IL-17 producing-CD4+T helper cell (Th17) differentiation. MST1 deficiency in DCs increases IL-17 production by CD4+T cells, whereas ectopic MST1 expression in DCs inhibits it. Notably, MST1-mediated DC-dependent Th17 differentiation regulates experimental autoimmune encephalomyelitis and antifungal immunity. Mechanistically, MST1-deficient DCs promote IL-6 secretion and regulate the activation of IL-6 receptor a/ß and STAT3 in CD4+T cells in the course of inducing Th17 differentiation. Activation of the p38 MAPK signal is responsible for IL-6 production in MST1-deficient DCs. Thus, our results define the DC MST1-p38MAPK signalling pathway in directing Th17 differentiation