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Leukocyte traffic to sites of inflammation
Author(s) -
JUTILA MARK A.
Publication year - 1992
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1992.tb00861.x
Subject(s) - selectin , cell adhesion molecule , microbiology and biotechnology , leukocyte trafficking , soluble cell adhesion molecules , integrin , inflammation , cell adhesion , endothelium , immunology , biology , endothelial stem cell , leukocyte extravasation , immune system , in vivo , intercellular adhesion molecule , adhesion , e selectin , function (biology) , in vitro , cell , chemistry , biochemistry , chemokine , genetics , organic chemistry
The adhesion of circulating leukocytes to the vascular endothelium is essential for effective host inflammatory and immune responses. Adhesion proteins expressed by both the leukocyte and endothelial cell have been well characterized, and studies of these molecules have shown that both cell types are actively involved in regulating these binding events. Most leukocyte (leukocyte integrins) and endothelial cell (vascular selectins, ICAM‐1, and VCAM) adhesion proteins increase in expression and function in response to mediators released by inflamed tissues. In contrast, the expression and function of one type of leukocyte molecule, L‐selectin (previously called LECAM‐1, LAM‐1, gp90MEL‐14), is “down‐regulated” by inflammatory signals. The purpose of this review is to summarize in vitro and in vivo regulatory and functional studies of some of the molecular mechanisms which regulate leukocyte‐endothelial cell adhesion, with particular emphasis on L‐selectin, and to present a hypothetical model of how these molecules may be orchestrated in vivo resulting in the control of host inflammatory responses.