Microparticle-induced release of B-lymphocyte regulators by rheumatoid synoviocytes.
Microparticle-induced release of B-lymphocyte regulators by rheumatoid synoviocytes.
复制标题
DOI：
10.1186/ar2648
复制
发表时间：
2009
影响因子：
4.9
通讯作者：
Wachsmann D
中科院分区：
文献类型：
--
作者：
Messer L;Alsaleh G;Freyssinet JM;Zobairi F;Leray I;Gottenberg JE;Sibilia J;Toti-Orfanoudakis F;Wachsmann D
在本研究中，我们研究了从类风湿性关节炎或骨关节炎患者滑液中分离出的微粒诱导类风湿成纤维细胞样滑膜细胞合成和释放B细胞激活因子、胸腺基质淋巴细胞生成素和分泌性白细胞蛋白酶抑制物的能力。对类风湿性关节炎、骨关节炎、微结晶性关节炎和反应性关节炎患者的滑液中的微粒进行了分析。此外，对不同细胞系(CEM淋巴细胞和THP-1细胞)激活后的微粒子释放进行了评估。采用差速离心法分离微粒，经固定化Annexin V捕获后，用凝血酶原酶法定量测定B细胞激活因子、胸腺基质淋巴生成素，用酶联免疫吸附试验检测分泌型白细胞蛋白水解酶抑制物的释放。从类风湿性关节炎和骨性关节炎患者滑液中分离出的微粒或来自活化的THP-1细胞的微粒能够诱导类风湿关节炎成纤维细胞样滑膜细胞释放B细胞激活因子、胸腺基质淋巴生成素和分泌性白细胞蛋白酶抑制物。反之，PHA、PMA和ADT-D联合作用产生的CEM淋巴细胞来源的微粒子不能促进B细胞激活因子的释放，但能促进类风湿关节炎成纤维细胞样滑膜细胞分泌胸腺基质淋巴生成素和分泌型白细胞蛋白酶抑制物。然而，从放线菌素D处理的CEM淋巴细胞中分离出的微粒不能诱导B细胞激活因子、胸腺基质淋巴生成素或分泌性白细胞蛋白酶抑制物的释放，这表明来自于凋亡T细胞的微粒在B细胞激活中不起效应作用。这些结果表明，微粒是一种信号结构，在触发的自身免疫诱导和放大过程中可能扮演特定的传送者的角色。这项研究还表明，微粒在B淋巴细胞和自身免疫靶细胞之间关于其来源的亲本细胞之间的串扰中具有不同的影响。
In the present study, we investigated the ability of microparticles isolated from synovial fluids from patients with rheumatoid arthritis or osteoarthritis to induce the synthesis and release of key cytokines of B-lymphocyte modulation such as B cell-activating factor, thymic stroma lymphopoietin, and secretory leukocyte protease inhibitor by rheumatoid fibroblast-like synoviocytes. Microparticles were analyzed in synovial fluids from patients with rheumatoid arthritis, osteoarthritis, microcristalline arthritis, and reactive arthritis. In addition, microparticle release after activation from various cell lines (CEM lymphocyte and THP-1 cells) was assessed. Microparticles were isolated by differential centrifugation, and quantitative determinations were carried out by prothrombinase assay after capture on immobilized annexin V. B cell-activating factor, thymic stroma lymphopoietin, and secretory leukocyte protease inhibitor release was evaluated by enzyme-linked immunosorbent assay. Microparticles isolated from synovial fluids obtained from rheumatoid arthritis and osteoarthritis patients or microparticles derived from activated THP-1 cells were able to induce B cell-activating factor, thymic stroma lymphopoietin, and secretory leukocyte protease inhibitor release by rheumatoid arthritis fibroblast-like synoviocytes. Conversely, CEM-lymphocytes-derived microparticles generated by treatment with a combination of PHA, PMA and Adt-D did not promote the release of B cell-activating factor but favored the secretion of thymic stroma lymphopoietin and secretory leukocyte protease inhibitor by rheumatoid arthritis fibrobast-like synoviocytes. However, microparticles isolated from actinomycin D-treated CEM lymphocytes were not able to induce B cell-activating factor, thymic stroma lymphopoietin, or secretory leukocyte protease inhibitor release, indicating that microparticles derived from apoptotic T cells do not function as effectors in B-cell activation. These results demonstrate that microparticles are signalling structures that may act as specific conveyors in the triggered induction and amplification of autoimmunity. This study also indicates that microparticles have differential effects in the crosstalk between B lymphocytes and target cells of autoimmunity regarding the parental cells from which they derive.
登录
查看更多内容
影响因子：
--
作者：
Morel, Olivier;Toti, Florence;Freyssinet, Jean-Marie
通讯作者：
Freyssinet, Jean-Marie
DOI：
10.1161/01.atv.0000170133.43608.37
发表时间：
2005-07-01
影响因子：
8.7
作者：
Mause, SF;von Hundelshausen, P;Weber, C
通讯作者：
Weber, C
类风湿关节炎中滑膜细胞。滑膜成纤维细胞。
影响因子：
4.9
作者：
Mueller-Ladner, Ulf;Ospelt, Caroline;Gay, Steffen;Distler, Oliver;Pap, Thomas
通讯作者：
Pap, Thomas
影响因子：
15.9
作者：
Burger, JA;Zvaifler, NJ;Kipps, TJ
通讯作者：
Kipps, TJ
影响因子：
9.8
作者：
Andoh, A;Tsujikawa, T;Fujiyama, Y
通讯作者：
Fujiyama, Y