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Arterial and venular endothelial cell costimulation of cytokine secretion by human T cell clones
Author(s) -
Johnson David R.,
Hauser Ingeborg A.,
Voll Reinhard E.,
Emmrich Frank
Publication year - 1998
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.63.5.612
Subject(s) - biology , secretion , cytokine , endothelial stem cell , immunology , microbiology and biotechnology , endocrinology , in vitro , biochemistry
Vascular endothelial cell (EC) costimulation of cytokine secretion by T lymphocytes may be important in inflammation and allograft rejection. Venous and arterial iliac endothelial cells (VIEC, AIEC) both costimulate interleukin‐2 (IL‐2) production by peripheral blood lymphocytes (PBL) or T cell clones stimulated with phytohemagglutinin (PHA). Interferon‐γ (IFN‐γ) production is costimulated in a subset of clones but IL‐4 is not. Surprisingly, two T cell clones were reciprocally better costimulated by VIEC or AIEC. EC activation by pretreatment with tumor necrosis factor α (TNF‐α) does not increase T cell costimulation despite large increases in EC cell adhesion molecule expression. Neither VIEC nor AIEC express CTLA4‐binding molecules and costimulation is blocked by cyclosporin A, suggesting that CD28 is not involved in EC costimulation of T cells. These data suggest that adult vascular EC costimulate production of IL‐2 and IFN‐γ but not IL‐4 by mature T cells, that EC costimulation is not increased in inflamed tissues, and that different EC optimally costimulate particular T cells. These findings have implications for the nature of the costimulatory signal(s) provided by EC and may be important in understanding vasculitis or atherosclerosis. J. Leukoc. Biol . 63: 612–619; 1998.