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 im mune dysfunction, excessive lipid peroxidation, and malnutrition cause d by retrovirus infection, female C57BL/6 mice were infected with LP-B M5 retrovirus, Infection with retrovirus inhibited lymphocyte prolifer ation, cytokine release T helper 1 cells, stimulated cytokine secretio n by T helper 2 cells, induced abnormal hepatic and cardiac lipid prof iles, and produced excessive tissue lipid peroxidation with hepatic an d cardiac vitamin E deficiency, Two weeks after infection, TCR peptide s V beta 5.2, V beta 8.1, V beta 8.1 + V beta 5.2, V beta 8.1(N), and V beta 8.1(C) were injected to the mice at dose of 200 mu g/ mouse. V beta 8.1 and V beta 5.2 treatments largely maintained lymphocyte proli feration and IL-2 and lFN-gamma release, and prevented excessive IL-6, IL-10, and TNF-alpha secretion. Concomitantly, these treatments norma lized hepatic and cardiac lipid profiles, reduced tissue lipid peroxid ation, and thereby significantly maintained vitamin E in the liver and heart, V beta 8.1 segments treatment did not prevent the immune dysfu nction, abnormal lipid profile and lipid peroxidation, and vitamin E d eficiency caused by the retrovirus infection, In conclusion, injection of intact TCR peptides during murine retrovirus infection largely pre vented immune dysfunction by blocking the excessive stimulation of a T cell subset caused by retroviral superantigens. It also ameliorated m alnutrition status by normalizing lipid profile, lipid peroxidation, a nd vitamin E deficiency, T cell immune dysfunction and its prevention by TCR peptide treatment is important in the therapy of vitamin 5 defi ciency induced by retrovirus infection.