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The role of the graft endothelium in transplant rejection: Evidence that endothelial activation may serve as a clinical marker for the development of chronic rejection
Author(s) -
Denton Mark D.,
Davis Stacy F.,
Baum Michelle A.,
Melter Michael,
Reinders Marlies E. J.,
Exeni Andrea,
Samsonov Dmitry V.,
Fang Jim,
Ganz Peter,
Briscoe David M.
Publication year - 2000
Publication title -
pediatric transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 69
eISSN - 1399-3046
pISSN - 1397-3142
DOI - 10.1034/j.1399-3046.2000.00031.x
Subject(s) - allorecognition , endothelium , medicine , chemokine , major histocompatibility complex , immunology , endothelial activation , cell adhesion molecule , endothelial stem cell , transplantation , microbiology and biotechnology , chemokine receptor , inflammation , biology , antigen , genetics , in vitro
In this review, we discuss the role of the allograft endothelium in the recruitment and activation of leukocytes during acute and chronic rejection. We discuss associations among endothelial activation responses, the expression of adhesion molecules, chemokines and chemokine receptors, and rejection; and we propose that endothelial vascular cellular adhesion molecule‐1 (VCAM‐1) may be used as a surrogate marker of acute rejection and allograft vasculopathy. In addition, we describe potential mechanistic interpretations of persistent endothelial cell (EC) expression of major histocompatibility complex (MHC) class II molecules in allorecognition. The graft endothelium may provide an antigen‐specific signal to transmigrating, previously activated, T cells and may induce B7 expression on locally transmigrating leukocytes to promote costimulation. Taken together, these functions of the EC provide it with a potent regulatory role in rejection and in the maintenance of T‐cell activation via the direct and/or the indirect pathways of allorecognition.