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Antitumor Effect by Interleukin-11 Receptor -Locus Chemokine/CCL27, Introduced into Tumor Cells through a Recombinant Adenovirus Vector¹

Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871 [J-Q. G., Y. Tsud., K. K., Y. Tsut., T. M., S. N.]; Department of Microbiology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511 [T. N., O. Y.]; Department of Biomedical Science, DakoCytomation Company Ltd., Nishinotoin-higashiiru, Shijo-dori, Shimogyo, Kyoto 600-8493 [Y. H., Y. Ta.]; and Division of Cellular and Gene Therapy Products, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501 [H. M., T. H.], Japan

In this study, we examined antitumor activity of a mouse CC chemokine ILC/CCL27 and a mouse CX₃C chemokine fractalkine/CX₃CL1 in vivo. We generated recombinant adenovirus vectors with a fiber mutation, encoding mILC (Ad-RGD-mILC) and mFKN (Ad-RGD-mFKN). We confirmed tumor cells infected with Ad-RGD-mILC and Ad-RGD-mFKN to express and release these chemokines. Tumor rejection experiments in vivo were carried out by inoculating OV-HM cells infected with Ad-RGD-mILC or Ad-RGD-mFKN into immunocompetent mice. mILC significantly suppressed the tumor growth, whereas no such significant effect was observed by mFKN. The antitumor activity induced by mILC was T cell dependent, involving both CD4⁺ and CD8⁺ T cells. Immunohistochemical analysis revealed accumulation of both CD3⁺ lymphocytes and NK cells in the tumor tissue transduced with mILC and mFKN. However, there was a significant difference in the distribution of infiltrating cells. Furthermore, mFKN appeared to have an angiogenic activity, which might have masked its tumor suppressive activity. Collectively, ILC/CCL27 may be a good candidate molecule for cancer gene therapy.

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