As CCR3 is known to be expressed in T cells and involved in CD4+ and CD8+ T cell trafficking to inflammation and infiltration in the tumors [45,46], the induction of CCR3 expression by VEGF in T cells stimulated with anti-CD3 and anti-CD28 Abs suggests a novel mechanism by which tumor-derived VEGF could induce the migration of T cells into a tumor site, in addition to the direct effects of signals immediately downstream of the VEGFR-1 or VEGFR-2 receptors. Here, CD28 is linked to neoplasm.