Key result
Endothelial cell gp34 costimulates CD4+ T-cell proliferation and IL-2 production via OX40.
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We investigated whether gp34, the ligand of OX40, expressed on EC is involved in costimulation of T cells. Normal CD4+ T cells were stimulated with anti-CD3-coated beads, phytohemagglutinin (PHA), or concanavalin A (Con A) in the presence or absence of irradiated human umbilical vein endothelial cells (HUVEC). Stimulation of T cells with each of these mitogens results in significant T-cell proliferation only when HUVEC were present, and this proliferation was inhibited markedly by anti-OX40 or anti-gp34 monoclonal antibody (mAb). T cells cultured with HUVEC produced more interleukin (IL)-2 than those cultured without HUVEC. The addition of anti-IL-2R alpha chain and anti-IL-2R beta chain mAbs abolished the costimulatory effects of HUVEC. Thus, the augmentation of T-cell proliferation appears to be attributable to increased IL-2 production. These results suggest that gp34 expressed on HUVEC plays a role in potentiation of T-cell immune response by providing OX40+ T cells with costimulatory signals.
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Kunitomi et al. (2000) studied this question. Co-culture with irradiated human umbilical vein endothelial cells (HUVEC) and anti-OX40/anti-gp34 mAbs vs. Mitogen stimulation without HUVEC was evaluated on T-cell proliferation and IL-2 production. Endothelial cell gp34 costimulated CD4+ T-cell proliferation and IL-2 production via OX40 in vitro, an effect markedly inhibited by anti-OX40 or anti-gp34 monoclonal antibodies.
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