Regulation of CD4(+) T cells by pleural mesothelial cells via adhesion molecule-dependent mechanisms in tuberculous pleurisy.
Regulation of CD4(+) T cells by pleural mesothelial cells via adhesion molecule-dependent mechanisms in tuberculous pleurisy.
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DOI：
10.1371/journal.pone.0074624
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Shi HZ
中科院分区：
文献类型：
--
作者：
Yuan ML;Tong ZH;Jin XG;Zhang JC;Wang XJ;Ma WL;Yin W;Zhou Q;Ye H;Shi HZ
细胞间粘附分子-1（ICAM-1）和血管细胞粘附分子-1（VCAM-1）已被证明表达于胸膜间皮细胞（PMCs）上，并介导白细胞粘附和迁移;然而，关于粘附分子依赖性机制是否参与结核性胸腔积液（TPE）中PMCs对CD 4 + T细胞的调节尚不清楚。采用流式细胞术测定TPE中PMC上ICAM-1和VCAM-1的表达，以及CD 4 + T细胞上分别表达的ICAM-1和VCAM-1的反受体CD 11 a和CD 29的表达。探讨PMCs通过粘附分子依赖性机制对CD 4+辅助性T细胞亚群粘附、增殖、活化、选择性扩增的免疫调节作用。TPE组ICAM-1和VCAM-1 β阳性PMC细胞数较PMC组增加。IFN-γ增强ICAM-1的荧光强度，IL-4促进VCAM-1的表达。与外周血相比，TPE中CD 11 ahighCD 4+和CD 29 highCD 4 + T细胞的数量显著增加。用抗ICAM-1或抗VCAM-1 mAb预刺激PMCs可显著抑制PMCs诱导的粘附、活化以及效应调节性T细胞扩增。我们目前的数据表明，PMCs上的粘附分子途径调节CD 4 + T细胞的粘附和活化，并选择性地促进效应调节性T细胞的扩增。
Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) have been demonstrated to be expressed on pleural mesothelial cells (PMCs), and to mediate leukocyte adhesion and migration; however, little is known about whether adhesion molecule-dependent mechanisms are involved in the regulation of CD4+ T cells by PMCs in tuberculous pleural effusion (TPE). Expressions of ICAM-1 and VCAM-1 on PMCs, as well as expressions of CD11a and CD29, the counter-receptors for ICAM-1 and VCAM-1, respectively, expressed on CD4+ T cells in TPE were determined using flow cytometry. The immune regulations on adhesion, proliferation, activation, selective expansion of CD4+ helper T cell subgroups exerted by PMCs via adhesion molecule-dependent mechanisms were explored. Percentages of ICAM-1-positive and VCAM-1‒positive PMCs in TPE were increased compared with PMC line. Interferon-γ enhanced fluorescence intensity of ICAM-1, while IL-4 promoted VCAM-1 expression on PMCs. Percentages of CD11ahighCD4+ and CD29highCD4+ T cells in TPE significantly increased as compared with peripheral blood. Prestimulation of PMCs with anti‒ICAM-1 or ‒VCAM-1 mAb significantly inhibited adhesion, activation, as well as effector regulatory T cell expansion induced by PMCs. Our current data showed that adhesion molecule pathways on PMCs regulated adhesion and activation of CD4+ T cells, and selectively promoted the expansion of effector regulatory T cells.