Shin Jin-Young, Yoon Il-Hee, Kim Jung-Sik, Kim Bongi, Park Chung-Gyu
Department of Microbiology and Immunology, Tumor Immunity Medical Research Center, Cancer Research Institute, Seoul National University College of Medicine, South Korea.
Cell Immunol. 2009;256(1-2):72-8. doi: 10.1016/j.cellimm.2009.01.006. Epub 2009 Feb 26.
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.
血管内皮生长因子（VEGF）是一种促进肿瘤生长的促血管生成介质。VEGF在T淋巴细胞中的作用尚不清楚。我们发现，用抗CD3单克隆抗体（mAb）加抗CD28 mAb或抗原呈递细胞上的抗原激活的T淋巴细胞转录了VEGF受体1（VEGFR1）和VEGFR2的mRNA。然而，只有VEGFR1在T细胞表面表达。将VEGF添加到静止或活化的T细胞中均不影响其增殖，但VEGF增加了IL-10的产生并略微降低了IFN-γ的产生。趋化性分析表明，活化的T淋巴细胞对VEGF有迁移反应。我们的数据表明，VEGF对T细胞具有直接的免疫调节作用。高浓度的VEGF与T细胞上的VEGFR1结合可能会导致T细胞迁移至肿瘤部位，这种相互作用可能在肿瘤细胞介导的IL-10免疫逃逸中发挥作用。
