Wang Hui, Zhang Qian, Sun Yuankai, Tan Wenfeng, Zhang Miaojia
Department of Rheumatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China.
J Biomed Res. 2024 Nov 7;39(3):305-316. doi: 10.7555/JBR.38.20240244.
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.
脂联素受体1（ ）缺陷已被证明可抑制抗原诱导性关节炎小鼠中Th17细胞的分化，并减轻关节炎症和骨侵蚀。更多新出现的证据表明，Th17细胞可能分化为致病性（pTh17）和非致病性（npTh17）细胞，其中pTh17细胞在多种自身免疫和炎症性疾病中起关键作用。在本研究中，我们发现 缺陷抑制了pTh17细胞的分化，并诱导了pTh17细胞中的线粒体功能障碍。RNA测序显示，在 缺陷的CD4 T细胞中，与线粒体功能相关的基因 的表达水平显著增加。在 缺陷的CD4 T细胞中敲低 可部分逆转 缺陷对线粒体功能和pTh17细胞分化的影响。总之，本研究证明了 在调节线粒体功能以促进pTh17细胞分化方面的新作用，为自身免疫和炎症性疾病的潜在治疗靶点提供了一些见解。
