AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1.

Adiponectin receptor 1 ( ) deficiency has been shown to inhibit Th17 cell differentiation and reduce joint inflammation and bone erosion in antigen-induced arthritis mice. Additional emerging evidence indicates that Th17 cells may differentiate into pathogenic (pTh17) and non-pathogenic (npTh17) cells, with the pTh17 cells playing a crucial role in numerous autoimmune and inflammatory conditions. In the current study, we found that deficiency inhibited pTh17 differentiation and induced mitochondrial dysfunction in pTh17 cells. RNA sequencing demonstrated a significant increase in the expression levels of , a gene related to mitochondrial function, in -deficient CD4 T cells. knockdown in -deficient CD4 T cells partially reversed the effects of deficiency on mitochondrial function and pTh17 differentiation. In conclusion, the current study demonstrated a novel role of in regulating mitochondrial function to promote pTh17 cell differentiation, providing some insight into potential therapeutic targets for autoimmune and inflammatory diseases.