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Interactions between endothetial cells and leukocytes
Author(s) -
Butcher E. C.,
Lewinsohn D.,
Duijvestijn A.,
Bargatze R.,
Wu N.,
Jalkanen S.
Publication year - 1986
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240300204
Subject(s) - leukocyte extravasation , extravasation , lymphocyte homing receptor , homing (biology) , lymphokine , immune system , biology , immunology , inflammation , lymphocyte , microbiology and biotechnology , receptor , high endothelial venules , bone marrow , lymphatic system , cell type , cell , cell adhesion , ecology , biochemistry , genetics
We present evidence that specific receptors are utilized by neutrophils to control their interaction with endothelial cells at sites of acute inflammation and that these receptors are related if not identical to lymphocyte “homing receptors” for lymphoid tissue high endothelium. We speculate that such receptors play a fundamental but not exclusive role in controlling the extravasation and tissue localization of all bone marrow‐derived nucleated cells. In addition, we emphasize the active role of endothelial cells in the process of lymphocyte migration and leukocyte extravasation. By the expression of as yet unidentified organ‐specific determinants for lymphocyte recognition, endothelial cells control the exit of particular lymphocyte subsets into mucosal versus nonmucosal sites, thus helping to determine the unique features of mucosal versus nonmucosal immune responses. Furthermore, we argue that endothelial cells are exquisitely responsive to local immune reactivity and present evidence that specific lymphokines, including γ‐interferon, play an important role in inducing postcapillary venules to express differentiated features required for the support of lymphocyte traffic into lymphoid organs and into sites of chronic inflammation. Leukocytes, endothelial cells, and probably other tissue cell classes appear to interact at multiple levels by a variety of mechanisms to regulate the local extravasation of immune effector cells.