GPR183在系统性红斑狼疮患者外周血T和B细胞亚群中的异常低表达。

IF 3.3 4区 医学 Q3 IMMUNOLOGY
Autoimmunity Pub Date : 2022-11-01 Epub Date: 2022-07-25 DOI:10.1080/08916934.2022.2103119
Mingming Zhao, Yang Mei, Zhidan Zhao, Pengpeng Cao, Yue Xin, Yunkai Guo, Ming Yang, Haijing Wu
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引用次数: 2

摘要

G蛋白偶联受体183 (GPR183)已被证明在T细胞依赖性抗体反应中介导免疫细胞的迁移和定位。系统性红斑狼疮(SLE)是一种典型的自身免疫性疾病,涉及B细胞介导的耐受性破坏和过多的致病性自身抗体产生,其中多种gpcr起作用。迄今为止,关于GPR183在SLE患者淋巴细胞亚群中的表达尚无系统研究。在本研究中,我们首先观察了GRP183在人扁桃体组织中不同T细胞亚群和B细胞亚群中的表达趋势。这些淋巴细胞亚群包括CD4+、CD8+、naïve T、效应T、Tfh、活化Tfh、Th1、Th2、Th17、Treg、CD19+CD27-、CD19+CD27+、naïve B、生发中心B、记忆B和浆细胞。此外,与健康对照(hc)相比,SLE患者以上外周血淋巴细胞亚群中的GPR183表达水平总体降低。GPR183在SLE非活动性和活动性患者中的表达差异提示GPR183的表达可能与SLE的疾病活动性有关。与SLEDAI评分呈强负相关,与血清补体蛋白C3、C4、C1q水平呈正相关,进一步证实了这一点。进一步的受试者工作特征(ROC)曲线分析显示,GPR183在循环CD27-IgD+ B细胞中的表达可能有助于区分非活动性和活动性SLE患者。此外,I型干扰素刺激可下调外周血T和B细胞亚群中GPR183的表达。GPR183的异常表达可能为SLE的疾病活动预测和潜在发病机制提供一些新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Abnormal lower expression of GPR183 in peripheral blood T and B cell subsets of systemic lupus erythematosus patients.

G protein-coupled receptor 183 (GPR183) has been indicated to mediate the migration and localisation of immune cells in T cell-dependent antibody responses. Systemic lupus erythematosus (SLE) is a canonical autoimmune disease involving B cell-mediated tolerance destruction and excessive pathogenic autoantibody production, in which multiple GPCRs play a role. To date, there has been no systematic study regarding the expression of GPR183 in lymphocyte subsets of SLE patients. In this research, firstly, we observed the expression trends of GRP183 in various T and B cell subsets in human tonsil tissues. These lymphocyte subsets include CD4+, CD8+, naïve T, effector T, Tfh, activated Tfh, Th1, Th2, Th17, Treg, CD19+CD27-, CD19+CD27+, naïve B, germinal centre B, memory B, and plasma cells. Further, compared with healthy controls (HCs), GPR183 expression levels in above peripheral blood lymphocyte subsets of patients with SLE were reduced overall. The differential expression of GPR183 expression between inactive and active SLE patients indicates that GPR183 expression may be concerned with the disease activity of SLE. This was further confirmed through the strong negative correlation with SLEDAI score and positive correlation with serum complement protein C3, C4 and C1q levels. Further receiver operating characteristic (ROC) curve analysis revealed that GPR183 expression in circulating CD27-IgD+ B cells may be beneficial in distinguishing between inactive and active SLE patients. In addition, type I interferon stimulation could down-regulate the expression of GPR183 in peripheral blood T and B cell subsets. Aberrant expression of GPR183 may provide some novel insights into disease activity prediction and underlying pathogenesis of SLE.

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来源期刊
Autoimmunity
Autoimmunity 医学-免疫学
CiteScore
5.70
自引率
8.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.
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