CD31 expressed on distinctive T cell subsets is a preferential amplifier of β1 integrin-mediated adhesion

Yoshiya Tanaka, Steven M. Albelda, Kevin J. Horgan, Gijs A. Van Seventer, Yoji Shimizu, Walter Newman, John Hallam, Peter J. Newman, Clayton A. Buck, Stephen Shaw

Research output: Contribution to journalArticlepeer-review

338 Scopus citations

Abstract

The CD31 (platelet endothelial cell adhesion molecule-1 [PECAM-1]/endothelial cell adhesion molecule [endoCAM]) molecule expressed on leukocytes, platelets, and endothelial cells is postulated to mediate adhesion to endothelial ceUs and thereby function in immunity, inflammation, and wound healing. We report the following novel features of CD31 which suggest a role for it in adhesion amplification of unique T cell subsets: (a) engagement of CD31 induces the adhesive function of β1 and β2 integrins; (b) adhesion induction by CD31 immunoglobulin G (IgG) monoclonal antibodies (mAbs) is sensitive, requiring only bivalent mAb; (c) CD31 mAb induces adhesion rapidly, but it is transient; (d) unique subsets of CD4+ and CD8+ T cells express CD31, including all naive (CD45RA+) CD8 T cells; and (e) CD31 induction is selective, inducing adhesive function of β1 integrins, particularly very late antigen-4, more efhciently than the β2 integrin lymphocyte function-associated antigen-1. Conversely, CD3 is more effective in inducing β2-mediated adhesion. Taken together, these findings indicate that unique T cell subsets express CD31, and CD31 has the capacity to induce integrin-mediated adhesion of T cells in a sensitive and selective fashion. We propose that, in collaboration with other receptors/ ligands, CD31 functions in an “adhesion cascade“ by amplifying integrin-mediated adhesion of CD31+ T cells to other cells, particularly endothelial calls.

Original languageEnglish (US)
Pages (from-to)245-253
Number of pages9
JournalJournal of Experimental Medicine
Volume176
Issue number1
DOIs
StatePublished - Jul 1 1992

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