Vascular endothelial growth factor-induced chemotaxis and IL-10 from T cells

Abstract

Vascular endothelial growth factor (VEGF) is a proangiogenic mediator that promotes tumor growth. The role of VEGF in T lymphocytes is unknown. We found that T lymphocytes activated by either anti-CD3 monoclonal antibody (mAb) plus anti-CD28 mAb or by antigens on antigen-presenting cells transcribed mRNA for VEGF receptor 1 (VEGFR1) and VEGFR2. However, only VEGFR1 was expressed on the T cell surface. The addition of VEGF to either resting or activated T cells did not affect their proliferation, but VEGF increased IL-10 production and slightly decreased IFN-gamma production. A chemotaxis assay revealed that activated T lymphocytes migrate in response to VEGF. Our data suggest that VEGF has a direct immunomodulatory effect on T cells. Engagement of a high concentration of VEGF with VEGFR1 on T cells may cause T cells to migrate to tumor sites, and this interaction may play a role in IL-10-mediated immune evasion by tumor cells.