关节炎中免疫细胞-软骨的相互作用

Y. Xiang, Tomohiro Kato
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引用次数: 0

摘要

关节炎被证实与软骨组织自身免疫有关。本文综述了软骨组织自身抗原与免疫细胞在关节炎中对这些分子的特异性反应中的相互作用。软骨组织自身抗原来源不同,在关节炎发病过程中发挥的作用也不同。成纤维滑膜细胞和软骨细胞也可以向抗原特异性T细胞以及滑膜巨噬细胞、树突状细胞和B细胞呈递抗原。CD4+ T细胞在类风湿关节炎中起关键作用,而CD8+ T细胞在血清阴性颈椎病中起主导作用。Th1/Th2和Th-/ t调节细胞失衡与疾病的发生和维持有关。最近的研究表明,B细胞通过特异性抗原的呈递、t细胞活性的调节、促炎细胞因子的分泌和自身抗体的产生,参与软骨破坏。软骨和免疫细胞之间的相互作用在关节炎中起着关键作用。软骨组织的自身抗原、抗原呈递细胞、T细胞和B细胞是软骨破坏的主要参与者。恢复Th1/Th2和Th-/ t调节细胞的平衡以及B细胞的消耗可能是关节炎治疗的新课题。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immune-cell–cartilage interactions in arthritis
Arthritis is demonstrated in association with autoimmunity to cartilage tissue. This review discusses interaction between autoantigens from cartilage tissue and the immune cells in specific responses to these molecules in arthritis. The autoantigens from cartilage tissue play different roles in the pathogenesis of arthritis dependent on their different sources. Fibroblastic synovial cells and chondrocytes can also present antigens to antigen-specific T cells as well as synovial macrophages, dendritic cells and B cells. CD4+ T cells play crucial roles in rheumatoid arthritis whereas CD8+ T cells play dominant roles in seronegative spondylarthropathies. The Th1/Th2 and Th-/T-regulatory cell imbalance is associated with initiation and maintenance of the diseases. Recent research has revealed that B cells contribute to cartilage destruction by means of specific antigen presentation, adjustment of T-cell activity, proinflammatory-cytokine secretion and autoantibody production. The interaction between cartilage and immune cells plays pivotal roles in arthritis. Autoantigens from cartilage tissue, antigen-presenting cells, T cells and B cells are major players in cartilage destruction. Recovery of the balance of Th1/Th2 and Th-/T-regulatory cells as well as depletion of B cells may be new topics of therapy for arthritis.
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