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Journal of Virology, January 2000, p. 428-435, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Development of Human T-Cell Leukemia Virus Type 1-Transformed Tumors in Rats following Suppression of T-Cell Immunity by CD80 and CD86 Blockade

Shino Hanabuchi,1 Takashi Ohashi,1 Yoshihiro Koya,1 Hirotomo Kato,1,2 Fumiyo Takemura,1,3 Katsuiku Hirokawa,4 Takashi Yoshiki,5 Hideo Yagita,3,6 Ko Okumura,3,6 and Mari Kannagi1,3,*

Departments of Immunotherapeutics1 and Pathology and Immunology,4 Tokyo Medical and Dental University, Medical Research Division, Department of Veterinary Internal Medicine, Faculty of Agriculture, University of Tokyo,2 and Department of Immunology, Juntendo University School of Medicine,6 Tokyo 113, CREST, Japan Science and Technology Corporation, Saitama 332,3 and Department of Pathology, Hokkaido University School of Medicine, Sapporo 060,5 Japan

Received 14 April 1999/Accepted 21 September 1999

Host immunity influences clinical manifestations of human T-cell leukemia virus type 1 (HTLV-1) infection. In this study, we demonstrated that HTLV-1-transformed tumors could develop in immunocompetent rats by blocking a costimulatory signal for T-cell immune responses. Four-week-old WKA/HKm rats were treated with monoclonal antibodies (MAbs) to CD80 and CD86 and subcutaneously inoculated with syngeneic HTLV-1-infected TARS-1 cells. During MAb treatment for 14 days, TARS-1 inoculation resulted in the development of solid tumors at the site of inoculation, which metastasized to the lungs. In contrast, rats not treated with MAbs promptly rejected tumor cells. Splenic T cells from MAb-treated rats indicated impairment of proliferative and cytotoxic T-lymphocyte responses against TARS-1 in vitro compared to untreated rats. However, tumors grown in MAb-treated rats regressed following withdrawal of MAb therapy. Recovery of TARS-1-specific T-cell immune responses was associated with tumor regression in these rats. Our results suggest that HTLV-1-specific cell-mediated immunity plays a critical role in immunosurveillance against HTLV-1-transformed tumor development in vivo.

* Corresponding author. Mailing address: Department of Immunotherapeutics, Tokyo Medical and Dental University, Medical Research Division, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113, Japan. Phone: 81 (3) 5803-5798. Fax: 81 (3) 5803-0235. E-mail: kann.impt{at}med.tmd.ac.jp.

Journal of Virology, January 2000, p. 428-435, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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