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.
Liang
B
B
Arizona Prevention Center, University of Arizona, Tucson 85724, USA.
Zhang
Z
Z
Araghiniknam
M
M
Eskelson
C
C
Watson
R R
RR
D000595:Amino Acid Sequence; D000818:Animals; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology; D009206:Myocardium / Q000378:metabolism; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000502:physiology*; D012192:Retroviridae Infections / Q000276:immunology* / Q000378:metabolism; D014811:Vitamin E Deficiency / Q000517:prevention & control*
D016207:Cytokines; D016693:Receptors, Antigen, T-Cell, alpha-beta