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© Research
Publication : European journal of immunology

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in European journal of immunology - 01 Apr 1996

Zocchi MR, Ferrero E, Leone BE, Rovere P, Bianchi E, Toninelli E, Pardi R

Link to Pubmed [PMID] – 8625965

Eur. J. Immunol. 1996 Apr;26(4):759-67

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-1 dull 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-1 bright CD45RO+) 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-delta cyto), 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.

http://www.ncbi.nlm.nih.gov/pubmed/8625965