Premium
Focal effects of mononuclear leukocyte transendothelial migration: TNF‐α production by migrating monocytes promotes subsequent migration of lymphocytes
Author(s) -
Jong Andrew L.,
Green David M.,
Trial JoAnn,
Birdsall Holly H.
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.60.1.129
Subject(s) - microbiology and biotechnology , tumor necrosis factor alpha , biology , endothelium , cell adhesion molecule , secretion , endothelial stem cell , immunology , adhesion , cytokine , intercellular adhesion molecule 1 , cell adhesion , intracellular , cell , chemistry , in vitro , biochemistry , endocrinology , organic chemistry
In many inflammatory diseases, mononuclear leukocytes (MNLs) accumulate as focal infiltrates in perivascular spaces. We postulated that MNLs migrating through endothelium modify the microenvironment to promote the subsequent migration of additional MNLs into the same area. We found that as monocytes adhere to and migrate spontaneously through an endothelial monolayer, they secrete tumor necrosis fector‐α (TNF‐α) and interleukin‐1. These cytokines stimulate endothelial cell expression of CD54 (intercellular adhesion molecule‐1) and CD106 (vascular cell adhesion molecule‐1). Consequently, when freshly isolated MNLs are added to that endothelial monolayer four or more hours later, significantly greater numbers of lymphocytes bind to and migrate through these endothelial monolayers. In addition to its ability to activate endothelial cell adhesion molecules, TNF‐α induced directed migration of lymphocytes through collagen pads. These results illustrate a potential amplification mechanism by which MNLs moving through a vessel wall may secrete TNF‐α, leading to the recruitment of additional leukocytes into the same perivascular locus.