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[Cancer Research 59, 3128-3133, July 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 3128-3133, July 1, 1999]
© 1999 American Association for Cancer Research

Immunology

Tumor Rejection by in Vivo Administration of Anti-CD25 (Interleukin-2 Receptor {alpha}) Monoclonal Antibody1

Shozaburo Onizuka, Isao Tawara, Jun Shimizu, Shimon Sakaguchi, Teizo Fujita and Eiichi Nakayama2

Department of Parasitology and Immunology, Okayama University Medical School, Okayama 700-8558 [S. O., I. T., E. N.]; Department of Oncology, Nagasaki University School of Medicine, Nagasaki 852-8523 [S. O.]; Department of Immunopathology, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo 173-0015 [J. S., S. S.]; and Department of Biochemistry, Fukushima Medical College, Fukushima 960-1295 [T. F.], Japan

Immune regulation has been shown to be involved in the progressive growth of some murine tumors. In this study, we demonstrated that a single in vivo administration of an amount less than 0.125 mg of anti-CD25 interleukin 2 receptor {alpha} monoclonal antibody (mAb; PC61) caused the regression of tumors that grew progressively in syngeneic mice. The tumors used were five leukemias, a myeloma, and two sarcomas derived from four different inbred mouse strains. Anti-CD25 mAb (PC61) showed an effect in six of the eight tumors. Administration of anti-CD25 mAb (PC61) caused a reduction in the number of CD4+CD25+ cells in the peripheral lymphoid tissues. The findings suggested that CD4+CD25+ immunoregulatory cells were involved in the growth of those tumors. Kinetic analysis showed that the administration of anti-CD25 mAb (PC61) later than day 2 after tumor inoculation caused no tumor regression, irrespective of depletion of CD4+CD25+ immunoregulatory cells. Two leukemias, on which the PC61-treatment had no effect, seemed to be incapable of eliciting effective rejection responses in the recipient mice because of low or no antigenicity.




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