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CD305 参与 RA 患者记忆性 CD4 T 细胞的异常激活,并减轻胶原诱导性关节炎。

CD305 participates in abnormal activation of memory CD4 T cells in patients with RA and attenuates collagen-induced arthritis.

机构信息

Department of Immunology, Xi'an Medical University, Xi'an, Shaanxi, China.

Affiliated Baoji Hospital of Xi'an Medical University, Xi'an, Shaanxi, China.

出版信息

Mol Immunol. 2024 Sep;173:80-87. doi: 10.1016/j.molimm.2024.07.010. Epub 2024 Jul 29.

DOI:10.1016/j.molimm.2024.07.010
PMID:39079337
Abstract

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that mainly affects the joints. Studies have shown that memory CD4 T cells play an important role in the pathogenesis of RA. This study investigated the expression and function of CD305 on human memory CD4 T cells and the effects of CD305 activating antibody on collagen-induced arthritis. The results showed that CD305 expression was significantly decreased on circulating memory CD4 T cells from patients with RA and its mean fluorescence intensity (MFI) was negatively correlated with DAS28. Moreover, CD305 inhibited the activation of memory CD4 T cells by down-regulating CD69 and CD25 and the production of IFN-γ, IL-4, and IL-17A induced by anti-CD3/CD28 antibodies. In addition, activation of CD305 inhibited the severity of disease in collagen-induced arthritis. In summary, CD305 reduction may mediate the excessive activation of memory CD4 T cells and participate in the development of RA. It can be used as a predictive marker of disease activity and has potential medicinal value in the treatment of RA.

摘要

类风湿关节炎(RA)是一种主要影响关节的慢性系统性自身免疫性疾病。研究表明,记忆 CD4 T 细胞在 RA 的发病机制中起重要作用。本研究探讨了人类记忆 CD4 T 细胞上 CD305 的表达和功能,以及 CD305 激活抗体对胶原诱导性关节炎的影响。结果表明,RA 患者循环记忆 CD4 T 细胞上 CD305 的表达显著降低,其平均荧光强度(MFI)与 DAS28 呈负相关。此外,CD305 通过下调 CD69 和 CD25 以及抑制抗 CD3/CD28 抗体诱导的 IFN-γ、IL-4 和 IL-17A 的产生来抑制记忆 CD4 T 细胞的活化。此外,CD305 的激活抑制了胶原诱导性关节炎的疾病严重程度。总之,CD305 的减少可能介导记忆 CD4 T 细胞的过度活化,并参与 RA 的发生发展。它可以作为疾病活动的预测标志物,在 RA 的治疗中具有潜在的药用价值。

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Mol Immunol. 2024 Sep;173:80-87. doi: 10.1016/j.molimm.2024.07.010. Epub 2024 Jul 29.
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