Complex regulation of granulocyte adhesion to cytokine-activated endothelium.
The adhesion of leukocytes to the endothelium is a hallmark in the development of an inflammation. Adhesion is caused by a number of mechanisms that depend upon the activation of the endothelium. The adhesion has to be specific for the different leukocyte types. I review here recent data with respect to polymorphonuclear granulocytes (PMN) adhesion to the endothelium of an inflammatory site. I especially focus on the pivotal role of Interferon gamma in the regulation of PMN adhesion to the endothelium. It modulates the adhesion of PMN caused by activation by other cytokines like IL-1, but does not affect the cell surface expression of the known adhesion molecules. I postulate the existence of a new class of cell surface modulators of adhesion which participate in the multiple step process of cell-cell adhesion.
Hallmann
R
R
Klinische Arbeitsgruppen für Rheumatologie der Max-Planck-Gesellschaft am Institut für experimentelle Medizin, Universität Erlangen-Nürnberg, Germany.
D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D016207:Cytokines / Q000494:pharmacology / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*
D016207:Cytokines; D007371:Interferon-gamma