Identification of subsets of human T cells capable of enhanced transendothelial migration.
Identification of subsets of human T cells capable of enhanced transendothelial migration.
复制标题
鉴定能够增强跨内皮迁移的人类 T 细胞亚群。
DOI：
10.4049/jimmunol.149.4.1170
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发表时间：
1992
影响因子：
4.4
通讯作者：
N. Oppenheimer
中科院分区：
文献类型：
--
作者：
Peter Pietschmann;J. Cush;P. Lipsky;N. Oppenheimer
免疫介导的炎症中的关键步骤是T细胞在毛细血管后微静脉的内皮细胞之间迁移并进入组织。为了确定特定细胞是否能够跨内皮迁移，检索并分析了已经迁移通过内皮单层的T细胞。为了实现这一点，将人脐静脉内皮细胞（EC）在胶原凝胶上培养至汇合，并与人T细胞一起孵育。单独收获不粘附于EC的T细胞、与内皮结合的T细胞以及已迁移通过内皮单层并进入胶原的细胞并进行表征。与EC孵育4小时后，T细胞自身分布为77 +/-2%为非粘附性，13 +/-2%与EC结合，10 +/-1%迁移至胶原中。迁移到胶原中的CD4 + T细胞主要是CD29bright/CD45RObright和CD45RA-。CD8 + T细胞表现出比CD4 + T细胞更大的跨内皮迁移能力。迁移的CD8 + T细胞主要为CD29bright，而CD45RA+。迁移细胞的额外表型分析表明，它们含有较少的表达L-选择素的细胞。此外，CD7的表面表达在已经迁移的T细胞中比在非粘附T细胞中密度低。最后，迁移的T细胞不富集CD45RBdim T细胞。延长EC孵育时间至36 h增加了迁移的T细胞数量，但并未改变迁移人群中CD29亮T细胞的优势。用IL-1或IFN-γ刺激EC也分别增加粘附和迁移T细胞的数量，但不改变迁移细胞的表型。这些结果表明，跨内皮迁移的能力是T细胞的某些亚群的内在能力，并与它们的分化阶段，如由它们的表面表型所确定的。
A critical step in immunologically mediated inflammation is the migration of T cells between endothelial cells of postcapillary venules and into the tissues. To determine whether specific cells are capable of transendothelial migration, T cells that had migrated through endothelial monolayers were retrieved and analyzed. To accomplish this, human umbilical vein endothelial cells (EC) were cultured to confluence on collagen gels and incubated with human T cells. T cells that were nonadherent to the EC, those that bound to the endothelium, and cells that had migrated through the endothelial monolayer and into the collagen were individually harvested and characterized. After a 4-h incubation with EC, T cells distributed themselves such that 77 +/- 2% were nonadherent, 13 +/- 2% were bound to EC, and 10 +/- 1% had migrated into the collagen. The CD4+ T cells that had migrated into the collagen were predominantly CD29bright/CD45RObright and CD45RA-. CD8+ T cells demonstrated a greater transendothelial migratory capacity than the CD4+ T cells. The migrated CD8+ T cells were mainly CD29bright but CD45RA+. Additional phenotypic analysis of the migrating cells indicated that they contained fewer cells that expressed L-selectin. Moreover the surface expression of CD7 was less dense in the T cells that had migrated than in the nonadherent T cells. Finally the T cells that migrated were not enriched for CD45RBdim T cells. Prolonging the incubation with EC to 36 h increased the number of T cells that migrated but did not alter the predominance of CD29bright T cells in the migrated population. Stimulation of EC with IL-1 or IFN-gamma also increased the number of adherent and migrating T cells, respectively, but did not alter the phenotype of the migrating cells. These results indicate that the capacity for transendothelial migration is an intrinsic ability of certain subpopulations of T cells and is related to their stage of differentiation as identified by their surface phenotype.