Chemokines have the potential to alter local immune responses by recruiting specific subsets of immune cells. Mice transgenic for epidermal expression of the HPV16 viral oncoprotein E7 driven by keratin 14 promoter (K14.E7) mimic chronic HPV infection and display increased lymphocytic infiltrate, epidermal hyperplasia and suppressed local immunity. We show here that chemokines CXCL9 and CXCL10 are highly expressed in non-haematopoietic cells in the skin of K14.E7 mice relative to non-transgenic skin, and recruit CXCR3⁺ T lymphocytes to the hyperplastic skin. Expression of CXCL9 and CXCL10 is not increased in E7-expressing mice with disrupted E7-Rb (Retinoblastoma) binding capability (K14.E7xRb^ΔL/ΔL) when compared with non-transgenic mice. Supernatants from K14E7 skin cultures preferentially promote migration of subsets of CXCR3⁺ T cells in vitro, and migration is inhibited by antibodies to CXCL9 and 10.  Furthermore, CXCR3 blockade by small molecule prevents rejection of E7-expressing but T cell deficient skin grafts. Taken together, the data suggest that increased expression of chemokines as a consequence of HPV-associated hyperplasia influence local immune responses in E7 transgenic skin, and hyperplasia-dependent factors could then potentially serve as targets for improving therapeutic vaccine development against chronic HPV infection.