@article {7639,
	title = {VEGF directly suppresses activation of T cells from ascites secondary to ovarian cancer via VEGF receptor type 2},
	journal = {British Journal of Cancer},
	volume = {107},
	year = {2012},
	note = {Cited By :27Export Date: 21 February 2017},
	month = {2012},
	pages = {1869 - 1875},
	abstract = {Background:Vascular endothelial growth factor action in tumour angiogenesis is well characterised; nevertheless, it functions as a key element in the promotion of the immune systems evasion by tumours. We sought to investigate the possible direct effect of VEGF on T-cell activation and through which type of VEGF receptor it exerts this effect on cells isolated from ovarian cancer patients ascites.Methods:T cells isolated from the ascites of ovarian cancer patients were cultured with anti-CD3 and IL-2, with or without VEGF for 14 days and the number of viable T cells was counted. Cytotoxic activity of cultured T cells and expression of VEGF receptor-2 (VEGFR-2), was assayed.Results:The addition of VEGF in cultures significantly reduced the number and proliferation rate of T cells in a dose-dependent manner and CD3 T cells expressed VEGFR-2 on their surface upon activation. Experiments with specific anti-VEGFR-2 antibodies revealed that the direct suppressive effect of VEGF on T-cell proliferation is mediated by VEGFR-2. We also showed that VEGF significantly reduced the cytotoxic activity of T cells.Conclusion:Our study showed that ascites-derived T cells secrete VEGF and express VEGFR-2 upon activation. Vascular endothelial growth factor directly suppresses T-cell activation via VEGFR-2. {\textcopyright} 2012 Cancer Research UK.},
	keywords = {EGFR-2, immune suppression, Ovarian cancer, T cells, VEGF},
	url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84870013053\&doi=10.1038\%2fbjc.2012.468\&partnerID=40\&md5=022a541dae24304f202fbc3cf934be55},
	author = {Gavalas, N.G. and Tsiatas, M. and Tsitsilonis, O. and Politi, E. and Ioannou, K. and Ziogas, A.C. and Rodolakis, A. and Vlahos, G. and Thomakos, N. and Haidopoulos, D. and Terpos, E. and Antsaklis, A. and Dimopoulos, M.A. and Bamias, A.}
}
