Increased Complement 3a Receptor is Associated with Behcet's disease and Vogt-Koyanagi-Harada disease.
Increased Complement 3a Receptor is Associated with Behcet's disease and Vogt-Koyanagi-Harada disease.
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补体 3a 受体增加与白塞病和沃格特-小柳-原田病相关
DOI：
10.1038/s41598-017-15740-8
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发表时间：
2017-11-14
影响因子：
4.6
通讯作者：
Yang P
中科院分区：
文献类型：
--
作者：
Wang C;Cao S;Zhang D;Li H;Kijlstra A;Yang P
白塞病(BD)和Vogt-Koyanagi-Harada病(VKH)是与T细胞免疫反应异常相关的全身性和复发性自身免疫性疾病。补体3a受体(C3aR)和补体5a受体(C5aR)参与T细胞介导的自身免疫性疾病。本研究旨在探讨C3aR和C5aR在这两种疾病中的作用。活动期BD(ABD)和活动期VKH(AVKH)患者PBMC C3aR表达增加。ABD和aVKH患者PBMC中C5aR的表达与正常对照组比较差异无统计学意义。BD和VKH患者眼内炎症控制后，C3aR表达恢复到正常水平。ABD和aVKH患者血清可显著诱导PBMCs表达C3aR。C3a刺激单核细胞分泌IL-6、IL-1β和肿瘤坏死因子-α，抑制IL-10的产生。CD4+T细胞C3aR的激活可上调IL-17的产生，抑制IL-10的产生，但对干扰素-γ的产生无明显影响。我们的数据表明，C3aR表达增加可能导致Th17细胞反应过度激活，从而可能参与BD和VKH疾病的发病机制。
Behcet’s disease (BD) and Vogt-Koyanagi-Harada disease (VKH) are systemic and recurrent autoimmune diseases associated with abnormal T cell immune response. Complement 3a receptor (C3aR) and complement 5a receptor (C5aR) have been reported to be involved in T cell mediated autoimmune disease. This study aimed to investigate the role of C3aR and C5aR in these two diseases. The C3aR expression in PBMCs was increased in patients with active BD (aBD) and active VKH (aVKH). No statistical difference was found concerning the expression of C5aR in PBMCs between patients with aBD or aVKH and normal controls. After the intraocular inflammation in BD and VKH patients was controlled, the C3aR expression returned back to normal levels. The serum from patients with aBD and aVKH significantly induced C3aR expression by PBMCs. C3a induced IL-6, IL-1β and TNF-α secretion, while inhibited the production of IL-10 by monocytes. Activation of C3aR in CD4+T cells could upregulate IL-17 production and inhibit IL-10 production, but had no detectable influence on IFN-γ production. Our data indicates that increased C3aR expression may lead to over activation of the Th17 cell response and may therefore contribute to the pathogenesis of BD and VKH disease.
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在 Vogt-Koyanagi-Harada 病中，IL-23 促进 CD4 T 细胞产生 IL-17。
影响因子：
14.2
作者：
Chi, Wei;Yang, Peizeng;Kijlstra, Aize
通讯作者：
Kijlstra, Aize
影响因子：
32.4
作者：
Strainic, Michael G.;Liu, Jinbo;Medof, M. Edward
通讯作者：
Medof, M. Edward
影响因子：
13.7
作者：
Yang, Peizeng;Ren, Yalin;Kijlstra, Aize
通讯作者：
Kijlstra, Aize
影响因子：
13.7
作者：
Yang, Peizeng;Fang, Wang;Kijlstra, Aize
通讯作者：
Kijlstra, Aize
影响因子：
27.4
作者：
Harry, Rachel A.;Anderson, Amy E.;Hilkens, Catharien M. U.
通讯作者：
Hilkens, Catharien M. U.