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Journal of Virology, July 2002, p. 7010-7019, Vol. 76, No. 14
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.14.7010-7019.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Correlation of Major Histocompatibility Complex Class I Downregulation with Resistance of Human T-Cell Leukemia Virus Type 1-Infected T Cells to Cytotoxic T-Lymphocyte Killing in a Rat Model

Takashi Ohashi,* Shino Hanabuchi, Reiko Suzuki, Hirotomo Kato, Takao Masuda, and Mari Kannagi

Department of Immunotherapeutics, Tokyo Medical and Dental University, Medical and Dental Research Division, Tokyo 113-8519, Japan

Received 6 November 2001/ Accepted 19 April 2002

Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) in infected individuals after a long incubation period. Despite the apparent transforming ability of HTLV-1 under experimental conditions, most HTLV-1 carriers are asymptomatic. These facts suggest that HTLV-1 is controlled by host immunity in most carriers. To understand the interplay between host immunity and HTLV-1-infected cells, in this study, we isolated several HTLV-1 Tax-specific cytotoxic T-lymphocyte (CTL) lines from rats inoculated with Tax-coding DNA and investigated the long-term effects of the CTL on syngeneic HTLV-1-infected T cells. Our results demonstrated that long-term mixed culture of these CTL and the virus-infected T cells led to the emergence of CTL-resistant HTLV-1-infected cells. Although the Tax expression level in these resistant cells was equivalent to that in the parental cells, expression of surface major histocompatibility complex class I (MHC-I) was significantly downregulated in the resistant cells. Downregulation of MHC-I was more apparent in RT1.Al, which presents a Tax epitope recognized by the CTL established in this study. Moreover, peptide pulsing resulted in killing of the resistant cells by CTL, indicating that resistance was caused by a decreased epitope density on the infected cell surface. This may be one of the mechanisms for persistence of HTLV-1-infected cells that evade CTL lysis and potentially develop ATL.

* Corresponding author. Mailing address: Department of Immunotherapeutics, Tokyo Medical and Dental University, Medical and Dental Research Division, 1-5-45 Yushima, Bunkyo-Ku, Tokyo 113-8519, Japan. Phone: 81 (3) 5803-5798. Fax: 81 (3) 5803-0235. E-mail: toha.impt{at}tmd.ac.jp.

Journal of Virology, July 2002, p. 7010-7019, Vol. 76, No. 14
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.14.7010-7019.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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