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Functional Consequences of Noncognate Interactions Between CD4⁺ Memory T Lymphocytes and the Endothelium¹

Lutz-Peter Berg^2,, Martha J. James^*, Montserrat Alvarez-Iglesias^*, Sarah Glennie^*, Robert I. Lechler^* and Federica M. Marelli-Berg^3,*

Departments of ^* Immunology and Histopathology, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom

The recruitment of Ag-specific T cells to sites of inflammation is a crucial step in immune surveillance. Although the molecular interactions controlling T cell extravasation are relatively well characterized, the effects of these events on T cell function are still poorly understood. Using an in vitro model of transendothelial migration of human CD4⁺ memory T cells, we have investigated the molecular and functional changes induced in T cells that come into contact with the endothelium. First, we show that transendothelial migration is precluded by signals that lead to T cell division. In addition, activation of the transcription factor AP-1, without induction of NF-B, is observed in T cells after noncognate interactions with endothelial cells (EC), a pattern of transcriptional regulation different from that observed in dividing T cells. Up-regulation of certain adhesion (CD11a, CD49d), activation (CD69), and costimulatory (CD86) receptors accompany these transcriptional events. Most importantly, recently migrated T cells display a faster rate of migration when reseeded onto an EC monolayer. Finally, T cells become hyperresponsive to antigenic challenge after noncognate interactions with the endothelium. These effects appear not to be due to the selection of preactivated T lymphocytes, because they occur also in clonal T cell populations and appear to be mediated by _L2 integrin-CD54 interactions. We conclude that CD4⁺ memory T cell extravasation is accompanied by phenotypic and functional changes induced by the interactions with the EC, which favor tissue infiltration by T cells and their further activation once they reach the antigenic site.

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