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Vitamin E Deficiency and Immune Dysfunction in Retrovirus-Infected C57BL/6 Mice Are Prevented by T-Cell Receptor Peptide Treatment^1,2,

Bailin Liang^*, Sussan Ardestani^*, Hsiao-Hui Chow, Cleamond Eskelson^** and Ronald R. Watson^*,3

^* Arizona Prevention Center Department of Pharmacy Practice ^** Department of Chemistry, University of Arizona, Tucson, AZ 85724

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine acquired immunodeficiency syndrome (AIDS), which is functionally similar to human AIDS. Retrovirus infection inhibited release of T-helper 1 cytokines, stimulated secretion of T-helper 2 cytokines and induced hepatic and cardiac vitamin E deficiency with increased lipid peroxides. We hypothesized that the immune dysfunction caused increased oxidation and loss of vitamin E. Because T-cell receptor (TCR) peptide treatment blocked the excessive stimulation of a T-cell subset by retroviral superantigens, we tested whether maintenance of normal immune function during infection prevented excessive oxidative damage. The TCR peptide treatments with doses > 100 µg/mouse and administered 2–4 wk postinfection significantly inhibited the retrovirus-induced immune dysfunction, concomitantly reduced tissue oxidative damage and thereby largely maintained vitamin E concentration in the liver and heart. Reducing the dose of peptide or delaying administration until early murine AIDS had developed resulted in severe immune dysfunction that caused elevated tissue lipid peroxidation and loss of vitamin E. The TCR peptide treatment partially maintained production of interleukin-2 (IL-2) and prevented retrovirus-induced elevated production of IL-6 by splenocytes in vitro. In conclusion, TCR peptide treatment during murine retrovirus infection ameliorated immune dysfunction and thus prevented increases in tissue lipid peroxidation and vitamin E loss. T-cell immune dysfunction and its prevention by TCR peptide treatment is important in the therapy of vitamin E deficiency induced by retrovirus infection.

KEY WORDS: • T-cell receptor • cytokine • vitamin E • murine AIDS • immune dysfunction • mice

¹ Appreciation is expressed for support by a Seed Money grant from the Office of the Vice President for Research, University of Arizona.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom reprint requests should be addressed.

Manuscript received 9 August 1995. Revision accepted 23 January 1996.