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Reduction of Retrovirus-Induced Immunosuppression by In Vivo Modulation of T Cells during Acute Infection

Hong He,^1, Ronald J. Messer,¹ Shimon Sakaguchi,² Guojun Yang,^1, Shelly J. Robertson,¹ and Kim J. Hasenkrug^1*

Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana,¹ Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan²

Received 3 March 2004/ Accepted 21 June 2004

Chronic infection with Friend retrovirus is associated with suppressed antitumor immune responses. In the present study we investigated whether modulation of T-cell responses during acute infection would restore antitumor immunity in persistently infected mice. T-cell modulation was done by treatments with DTA-1 anti- glucocorticoid-induced tumor necrosis factor receptor monoclonal antibodies. The DTA-1 monoclonal antibody is nondepleting and delivers costimulatory signals that both enhance the activation of effector T cells and inhibit suppression by regulatory T cells. DTA-1 therapy produced faster Th1 immune responses, significant reductions in both acute virus loads and pathology and, most importantly, long-term improvement of CD8⁺ T-cell-mediated antitumor responses.

Present address: Laboratory of Immunological Monitoring, Robert W. Franz Cancer Research Center, Providence Portland Medical Center, Portland, OR 97213-2967.

Present address: Laboratory of Cancer Immunobiology, Robert W. Franz Cancer Research Center, Providence Portland Medical Center, Portland, OR 97213-2967.

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