CD31/PECAM‐1‐driven chemokine‐independent transmigration of human T lymphocytes

CD31/PECAM‐1‐driven chemokine‐independent transmigration of human T lymphocytes
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CD31/PECAM-1驱动的不依赖趋化因子的人T淋巴细胞迁移

DOI:
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发表时间:
1996
影响因子:
5.4
通讯作者:
R. Pardi
R. Pardi
中科院分区:
医学3区
文献类型:
--
作者:
M. Zocchi;E. Ferrero;B. Leone;P. Rovere;E. Bianchi;E. Toninelli;R. Pardi

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我们使用稳定表达人CD 31/PECAM-1或细胞间粘附分子-1(CD 54/ICAM-1)的转染鼠成纤维细胞,评估了CD 31/PECAM-1(血小板内皮细胞粘附分子-1)对T淋巴细胞迁移的相对贡献。与CD 54/ICAM-1不同,CD 31/PECAM-1在不存在趋化因子的情况下支持活化T细胞的迁移:大多数迁移的淋巴细胞为CD 31+,并显示出对应于幼稚亚群的表型(LFA-1 dull和CD 45 RA+)。通过用趋化因子单核细胞趋化蛋白-1建立趋化梯度,可以诱导活化的T淋巴细胞穿过CD 54/ICAM-1+转染的单层细胞迁移,并且在这些条件下,迁移的细胞主要表现出记忆表型(LFA-1bright CD 45 RO+)。此外,我们发现在转染细胞中,CD 54/ICAM-1沿着细胞顶面均匀分布,而CD 31/PECAM-1集中在细胞间连接处,这表明存在与T细胞迁移有关的触针梯度(即基质或细胞结合分子的梯度)。这一点也得到了以下发现的证实:用缺乏胞质结构域的CD 31/PECAM-1突变体(CD 31/PECAM-1-Δcyto)转染的鼠成纤维细胞单层(其在细胞接触区域的定位倾向降低)支持有效粘附,但除非产生趋化梯度,否则无法诱导活化T细胞的迁移。我们认为,在淋巴细胞中,嗜同性CD 31/PECAM-1粘附可能主要参与幼稚T细胞的迁移,其作用与CD 54/ICAM-1的作用互补。
We assessed the relative contribution of CD31/PECAM‐1 (platelet‐endothelial cell adhesion molecule‐1) to T lymphocyte transmigration by the use of transfected murine fibroblasts stably expressing either the human CD31/PECAM‐1 or the intercellular adhesion molecule‐1 (CD54/ICAM‐1). Unlike CD54/ICAM‐1, CD31/PECAM‐1 supported migration of activated T cells in the absence of chemokines: most of the migrating lymphocytes were CD31+ and displayed a phenotype corresponding to the naive subpopulation (LFA‐1dull and CD45RA+). Migration of activated T lymphocytes through CD54/ICAM‐1+ transfected monolayers could be induced by creating a chemotactic gradient with the chemokine monocyte chemotactic protein‐1, and the migrating cells mainly displayed a memory phenotype (LFA‐1brightCD45RO+) under these conditions. Furthermore, we found that in transfected cells CD54/ICAM‐1 is uniformly distributed along the apical surface of the cells, while CD31/PECAM‐1 is concentrated at the intercellular junctions, suggesting the existence of a haptotactic gradient (i.e. a gradient of substrate‐ or cell‐bound molecules) responsible for T cell migration. This was also confirmed by the finding that monolayers of murine fibroblasts transfected with a CD31/PECAM‐1 mutant lacking the cytoplasmic domain (CD31/PECAM‐1‐Δcyto), which has a reduced tendency to localize at cell‐cell contact areas, supported efficient adhesion but were unable to induce migration of activated T cells unless a chemotactic gradient was created. We propose that in lymphocytes, homophilic CD31/PECAM‐1 adhesion may be primarily involved in transmigration of naive T cells and that its role is complementary to that of CD54/ICAM‐1.
DOI: 10.1172/jci113007
发表时间: 1987
期刊: The Journal of clinical investigation
影响因子: --
作者:
Bender,JR;Pardi,R;Karasek,MA;Engleman,EG
通讯作者: Engleman,EG
DOI: 10.4049/jimmunol.131.6.2895
发表时间: 1983-12
影响因子: 4.4
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通讯作者: P. Parham
DOI: 10.1182/blood.v84.7.2068.bloodjournal8472068
发表时间: 1994-10
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影响因子: 20.3
作者:
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DOI: 10.1073/pnas.91.9.3652
发表时间: 1994-04-26
影响因子: 11.1
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通讯作者: SPRINGER, TA
DOI: 10.1146/annurev.iy.10.040192.003021
发表时间: 1992
影响因子: 29.7
作者:
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通讯作者: L. Picker;E. Butcher