Prevention of Retrovirus-Induced Aberrant Cytokine Secretion, Excessive Lipid Peroxidation, and Tissue Vitamin E Deficiency by T Cell Receptor Peptide Treatments in C57BL/6 Mice

To test whether T cell receptor (TCR) peptide treatment can prevent immune dysfunction, excessive lipid peroxidation, and malnutrition caused by retrovirus infection, female C57BL/6 mice were infected with LP-BM5 retrovirus. Infection with retrovirus inhibited lymphocyte proliferation, cytokine release T helper 1 cells, stimulated cytokine secretion by T helper 2 cells, induced abnormal hepatic and cardiac lipid profiles, and produced excessive tissue lipid peroxidation with hepatic and cardiac vitamin E deficiency. Two weeks after infection, TCR peptides Vbeta5.2, Vbeta8.1, Vbeta8.1 + Vbeta5.2, Vbeta8.1(N), and Vbeta8.1 were injected to the mice at dose of 200 microg/mouse. Vbeta8.1 and Vbeta5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-gamma release, and prevented excessive IL-6, IL-10, and TNF-alpha secretion. Concomitantly, these treatments normalized hepatic and cardiac lipid profiles, reduced tissue lipid peroxidation, and thereby significantly maintained vitamin E in the liver and heart. Vbeta8.1 segments treatment did not prevent the immune dysfunction, abnormal lipid profile and lipid peroxidation, and vitamin E deficiency caused by the retrovirus infection. In conclusion, injection of intact TCR peptides during murine retrovirus infection largely prevented immune dysfunction by blocking the excessive stimulation of a T cell subset caused by retroviral superantigens. It also ameliorated malnutrition status by normalizing lipid profile, lipid peroxidation, and vitamin E deficiency. T cell immune dysfunction and its prevention by TCR peptide treatment is important in the therapy of vitamin E deficiency induced by retrovirus infection.