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树突状细胞- T 细胞相互作用在类风湿关节炎中的机制。

The mechanism of dendritic cell-T cell crosstalk in rheumatoid arthritis.

机构信息

School of Traditional Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, Gansu, 730000, China.

The First Clinical Medical College, Gansu University of Chinese Medicine, Lanzhou, Gansu, 730000, China.

出版信息

Arthritis Res Ther. 2023 Oct 5;25(1):193. doi: 10.1186/s13075-023-03159-8.

DOI:10.1186/s13075-023-03159-8
PMID:37798668
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10552435/
Abstract

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterised by joint pain and swelling, synovial hyperplasia, cartilage damage, and bone destruction. The mechanisms of dendritic cell (DC) and T cell-mediated crosstalk have gradually become a focus of attention. DCs regulate the proliferation and differentiation of CD4 T cell subtypes through different cytokines, surface molecules, and antigen presentation. DC-T cell crosstalk also blocks antigen presentation by DCs, ultimately maintaining immune tolerance. DC-T cell crosstalk mainly involves chemokines, surface molecules (TonEBP, NFATc1), the PD-L1/PD-1 signalling axis, and the TGF-β signalling axis. In addition, DC-T cell crosstalk in RA is affected by glycolysis, reactive oxygen species, vitamin D, and other factors. These factors lead to the formation of an extremely complex regulatory network involving various mechanisms. This article reviews the key immune targets of DC-T cell crosstalk and elucidates the mechanism of DC-T cell crosstalk in RA to provide a basis for the treatment of patients with RA.

摘要

类风湿关节炎(RA)是一种慢性炎症性疾病,其特征为关节疼痛和肿胀、滑膜增生、软骨损伤和骨破坏。树突状细胞(DC)和 T 细胞介导的串扰机制逐渐成为关注焦点。DC 通过不同的细胞因子、表面分子和抗原呈递来调节 CD4 T 细胞亚型的增殖和分化。DC-T 细胞串扰还阻止了 DC 对抗原的呈递,最终维持了免疫耐受。DC-T 细胞串扰主要涉及趋化因子、表面分子(TonEBP、NFATc1)、PD-L1/PD-1 信号轴和 TGF-β信号轴。此外,RA 中的 DC-T 细胞串扰受到糖酵解、活性氧、维生素 D 等因素的影响。这些因素导致了涉及各种机制的极其复杂的调节网络的形成。本文综述了 DC-T 细胞串扰的关键免疫靶点,并阐明了 DC-T 细胞串扰在 RA 中的作用机制,为 RA 患者的治疗提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/f5a093fb6dd0/13075_2023_3159_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/b26e75905749/13075_2023_3159_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/3eca1b1183e0/13075_2023_3159_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/f5a093fb6dd0/13075_2023_3159_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/b26e75905749/13075_2023_3159_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/21dc80e572cf/13075_2023_3159_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/3eca1b1183e0/13075_2023_3159_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/061e/10552435/f5a093fb6dd0/13075_2023_3159_Fig4_HTML.jpg

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