To test whether T tell receptor (TCR) peptide treatment can prevent immune dysfunction and malnutrition caused by retrovirus infection, female C57BL/6 mice were infected with I.P-BM5 retrovirus which caused murine AIDS. Retrovirus infection inhibited lymphocyte proliferation, T helper 1 cytokines release, stimulated T helper 2 cytokines secretion, caused hepatic Zn and Cu deficiency, induced abnormal hepatic and cardiac lipid profiles and excessive tissue lipid peroxidation with hepatic and cardiac vitamin E deficiency. TCR peptides VB5.2, VB3, VB3(1-11), and (5-16) were injected to the mice at dose of 200 ug/mouse two weeks after infection. V3 and VI15.2 treatments largely maintained lymphocyte proliferation, IL-2 and interferon-gamma release, prevented excessive IL-6 and IL-10 secretion, concomitantly normalized hepatic and cardiac lipid profiles and reduced tissue lipid peroxidation. and thereby significantly restored vitamin E in the liver and heart. VH3 segment treatments did not prevent the immune dysfunction, abnormal lipid profile and lipid peroxidation, and vitamin E deficiency caused by the retrovirus infection. In conclusion, intact TCR peptide treatments during murine retrovirus infection largely prevented immune dysfunction by blocking the excessive stimulation of a T cell subset caused by retroviral superantigens. and ameliorated malnutrition by normalizing lipid profile, lipid peroxidation. and vitamin E deficiency.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology