Journal of Leukocyte Biology, Vol 67, Issue 6 825-833, Copyright © 2000 by Society for Leukocyte Biology
JOURNAL ARTICLE |
Z Ding, K Xiong and TB Issekutz
Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada.
Human T lymphocyte transendothelial migration (TEM) was examined in response to chemokines across cytokine-activated endothelium. Monocyte chemotactic protein-1 (MCP-1), RANTES, and macrophage inflammatory protein-1alpha (MIP-1alpha) induced TEM by memory T cells, while stromal cell-derived factor-1 (SDF-1) induced TEM by both naive and memory T cells. Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) increased endothelial adhesion molecule (CAM) expression, whereas interferon-gamma (IFN-gamma) induced little up-regulation of CAM. However, both TNF-alpha and IFN-gamma strongly facilitated T cell migration, which was completely inhibited by pertussis toxin and both greatly increased TEM to RANTES, MIP-1alpha, and SDF-1 selectively of memory but not naive T cells. Thus, the dual selective effect on memory T cells of endothelial activation and these chemokines promotes the preferential recruitment of memory T cells to inflammatory sites. However, the enhanced chemokine-induced migration by memory T cells across activated endothelium appears to be independent of the increase in endothelial CAM expression. G-protein-linked stimuli may play an important part in T cell TEM across cytokine-activated endothelium.
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