肿瘤坏死因子α
类风湿性关节炎
免疫学
医学
癌症研究
受体
发病机制
自身免疫
关节炎
细胞因子
抗体
内科学
标识
DOI:10.54097/hset.v36i.6210
摘要
Rheumatoid arthritis (RA) induces articular damage through autoimmunity. Tumor necrosis factor-α (TNF-α) plays an important role in the pathogenesis of RA. TNF-α binds to its receptors to recruit certain molecules and forms two kinds of complexes (complex Ⅰ and Ⅱ) to regulate the pro-survival, apoptosis, and necrosis of cells. TNF-α upregulates RA by the methylation and acetylation of the RA synovial fibroblast gene and causes RA-derived joint damage through the induction of osteoclasts. Two TNF-α receptors mediate RA in opposite directions. TNF-α has been a target for the treatment of RA in which TNF-α inhibitors (TNFi) are administrated periodically for RA patients. Several mechanisms in the RA-related TNF-α signaling pathways remain imprecise including the regulation of regulatory T cells, osteoclast induction, and the potential interaction with the hypoxia-inducible factor. Further investigation into these questions may point out new methods for RA treatment to overcome the defects of current TNFi such as the anti-drug antibodies.
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