免疫调节分子在类风湿关节炎中的作用：对发病机制和治疗前景的影响,Journal of Cellular Physiology

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免疫调节分子在类风湿关节炎中的作用：对发病机制和治疗前景的影响
Journal of Cellular Physiology ( IF 4.5 ) Pub Date : 2022-08-08 , DOI: 10.1002/jcp.30855
Maryam Hemmatzadeh _{1,

2,

3} , Elham Ahangar Parvin ₄ , Hamed Mohammadi _{5,

6} , Gholamreza Azizi ₅ , Navid Shomali _{1,

2,

3} , Farhad Jadidi-Niaragh _{2,

3,

7}

Affiliation

类风湿性关节炎 (RA) 被认为是一种自身免疫性慢性疾病和最常见的炎症性关节病。RA 中的疾病进展始于具有遗传或环境倾向的无症状自身免疫反应，随着自身抗体到达关节而转变为关节痛期，受试者开始表现出缺乏滑膜炎症任何临床症状的非特异性肌肉骨骼表现。之后，患者的症状发展为未分化关节炎（UA）/特发性关节炎（IA），只要受试者进展为影响脉管系统、新陈代谢和骨骼的临床滑膜炎系统性合并症，最终随着免疫细胞浸润增强，IA/UA 患者就会进展临床可分类的 RA。RA主要与不同的免疫细胞相关，每种免疫细胞对疾病的发病机制都有不同的贡献。RA 的发病机制因 T 细胞和 B 细胞在自身免疫异常中的作用而改变。免疫反应的调节通过调节和抑制分子来控制适应性系统的激活以及免疫止血。为了限制过度的 T 细胞相关炎症反应，免疫系统提供了一个抑制反馈系统，统称为免疫检查点。在这篇综述中，我们旨在讨论免疫检查点分子的抑制性成员，包括程序性细胞死亡 1 (PD-1)/PD-L1、细胞毒性-T-淋巴细胞-抗原-4、淋巴细胞激活基因-3、T 细胞免疫球蛋白-3，T 细胞活化的 V 域 Ig 抑制因子，

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The role of immune regulatory molecules in rheumatoid arthritis: Implication for etiopathogenesis and prospective for treatment

Rheumatoid arthritis (RA) is considered an autoimmune chronic disorder and the most common inflammatory arthropathy. Disease progression in RA begins with asymptomatic autoimmune responses in cases with a genetic or environmental predisposition, that alters to arthralgia phase as autoantibodies reach the joints and subjects begin demonstrating nonspecific musculoskeletal presentations lacking any clinical symptoms of synovial inflammation. After that, patients' symptoms develop to undifferentiated arthritis (UA)/idiopathic arthritis (IA) whenever the subjects progress to clinical synovitis systemic comorbidities affecting the vasculature, metabolism, and bone, and eventually with augmented immune cell infiltration, IA/UA patients progress to clinically classifiable RA. RA is mainly correlated with different immune cells and each of them contributes variously to the pathogenesis of the disease. The pathogenesis of RA is altered by the contribution of both T and B cells in an autoimmune irregularity. Modulation of the immune responses occurs through regulatory and inhibitory molecules that control activation of the adaptive system as well as immune hemostasis. To confine the exorbitant T cell-associated inflammatory reactions, the immune system provides a system of inhibitory feedbacks, collectively named immune checkpoints. In this review, we aimed to discuss about inhibitory members of immune checkpoint molecules, including programmed cell death 1 (PD-1)/PD-L1, cytotoxic-T-lymphocyte-antigen-4, lymphocyte activation gene-3, T cell immunoglobulin-3, V-domain Ig suppressor of T cell activation, B- and T-lymphocyte attenuator, and T cell immunoglobulin and ITIM domain and their role in RA.

更新日期：2022-08-08

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