VLA-4-dependent and -independent pathways in cell contact-induced proinflammatory cytokine production by synovial nurse-like cells from rheumatoid arthritis patients
VLA-4-dependent and -independent pathways in cell contact-induced proinflammatory cytokine production by synovial nurse-like cells from rheumatoid arthritis patients
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类风湿性关节炎患者滑膜护理样细胞细胞接触诱导促炎细胞因子产生中的 VLA-4 依赖性和独立途径
DOI：
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
M. Miyasaka
中科院分区：
文献类型：
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作者：
E. Takeuchi;Toshiyuki Tanaka;E. Umemoto;T. Tomita;K. Shi;K. Takahi;R. Suzuki;T. Ochi;M. Miyasaka
来自类风湿性关节炎患者滑膜组织的护士样基质细胞系（RA-SNC）在与淋巴细胞共培养时产生大量促炎细胞因子。在本文中，我们分析了诱导RA-SNC细胞释放细胞因子所必需的分子事件，特别是细胞粘附和淋巴细胞的迁移（也称为假帝国）所起的作用。为此，使用克隆的RA-SNC系RA-SNC 77检查各种mAb对人B细胞系MC/car的结合和迁移的影响。为了分析淋巴细胞结合和迁移对RA-SNC 77细胞上调细胞因子产生的作用，我们使用C3外切酶处理的MC/car细胞，其可以结合RA-SNC 77细胞但不能迁移。用抗CD 29或抗CD 49 d mAb处理显著减少MC/car细胞的结合和迁移。相反，中和性抗CD 106/血管细胞粘附分子1 mAb未显示任何抑制作用。同样，抗CD 11 a、CD 18、CD 44、CD 49 e或CD 54的中和mAb均未显示显著作用。C3处理或未处理的MC/car细胞与RA-SNC 77细胞的结合诱导了相当水平的IL-6和IL-8产生。此外，RA-SNC 77细胞的细胞因子产生增强需要通过极晚期抗原-4（VLA-4）非依赖性粘附途径直接与淋巴细胞接触。这些结果表明，尽管VLA-4依赖性/血管细胞粘附分子1非依赖性和VLA-4非依赖性粘附途径都参与MC/car结合和随后的迁移，但只有VLA-4非依赖性粘附途径对于RA-SNC 77细胞增强的促炎细胞因子产生是必要和足够的。依赖于Rho-GTdR的轮回过程不是这种现象的先决条件。
Nurse-like stromal cell lines from the synovial tissue of patients with rheumatoid arthritis (RA-SNC) produce, on coculture with lymphocytes, large amounts of proinflammatory cytokines. In the present paper, we analyze the molecular events necessary for the induction of cytokine release from RA-SNC cells, and particularly the roles played by cell adhesion and the transmigration (also known as pseudoemperipolesis) of lymphocytes. For this purpose, the effects of various mAbs on the binding and transmigration of a human B-cell line, MC/car, were examined using a cloned RA-SNC line, RA-SNC77. To analyze the role of lymphocyte binding and transmigration on upregulated cytokine production by the RA-SNC77 cells, we used C3 exoenzyme-treated MC/car cells, which could bind to RA-SNC77 cells but could not transmigrate. Treatment with anti-CD29 or anti-CD49d mAb significantly reduced binding and transmigration of the MC/car cells. In contrast, the neutralizing anti-CD106/vascular cell adhesion molecule 1 mAb did not show any inhibitory effect. Likewise, none of the neutralizing mAbs against CD11a, CD18, CD44, CD49e, or CD54 showed significant effects. Binding of C3-treated or untreated MC/car cells to RA-SNC77 cells induced comparable levels of IL-6 and IL-8 production. In addition, the enhanced cytokine production by RA-SNC77 cells required direct lymphocyte contact via a very late antigen-4 (VLA-4)-independent adhesion pathway. These results indicate that, although both the VLA-4-dependent/vascular cell adhesion molecule 1-independent and the VLA4-independent adhesion pathways are involved in MC/car binding and subsequent transmigration, only the VLA4-independent adhesion pathway is necessary and sufficient for the enhanced proinflammatory cytokine production by RA-SNC77 cells. The transmigration process, which is dependent on Rho-GTPase, is not a prerequisite for this phenomenon.
骨髓成纤维细胞亚群支持 VLA-4 介导的 B 细胞前体迁移。
影响因子：
20.3
作者：
Tang,J;Scott,G;Ryan,DH
通讯作者：
Ryan,DH
胸腺护理细胞拯救早期 CD4 CD8 胸腺细胞免于凋亡。
DOI：
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发表时间：
1995
期刊：
Cellular and molecular biology (Noisy-le-Grand, France)
影响因子：
--
作者：
Pezzano,M;Li,Y;Philp,D;Omene,C;Cantey,M;Saunders,G;Guyden,JC
通讯作者：
Guyden,JC
影响因子：
15.9
作者：
Burger, JA;Zvaifler, NJ;Kipps, TJ
通讯作者：
Kipps, TJ