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AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1. | LitMetric
Adiponectin receptor 1 ( ) deficiency has been shown to inhibit Th17 cell differentiation and reduce joint inflammation and bone erosion in antigen-induced arthritis (AIA) 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 that the deletion of in pTh17 cells reduced the mitochondrial function. RNA-sequencing (RNA-seq) demonstrated a significant increase in the expression levels of , a gene related to mitochondrial function, in -deficient CD4 T cells. Interference with the expression in -deficient CD4 T cells partially mitigated the effect of deficiency on mitochondrial function and pTh17 differentiation. In conclusion, the current study demonstrated a novel role of AdipoR1 in regulating mitochondrial function FUNDC1 to promote pTh17 cell differentiation, providing some insights into potential therapeutic targets for autoimmune and inflammatory diseases.
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