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

Bailin Liang, Zhen Zhang, Mohsen Araghiniknam, Cleamond Eskelson, Ronald R Watson

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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 Vβ5.2, Vβ8.1, Vβ8.1 + Vβ5.2, Vβ8.1(N), and Vβ8.1 were injected to the mice at dose of 200 μg/mouse. Vβ8.1 and Vβ5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-γ release, and prevented excessive IL-6, IL- 10, and TNF-α 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. Vβ8.1 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.

Original languageEnglish (US)
Pages (from-to)87-94
Number of pages8
JournalProceedings of the Society for Experimental Biology and Medicine
Volume214
Issue number1
StatePublished - Jan 1997

Fingerprint

Vitamin E Deficiency
Retroviridae Infections
Retroviridae
T-Cell Antigen Receptor
Vitamin E
Inbred C57BL Mouse
Lipid Peroxidation
Tissue
Cytokines
Lipids
Peptides
Liver
Malnutrition
Therapeutics
T-cells
Lymphocytes
Superantigens
Th2 Cells
Th1 Cells
T-Lymphocyte Subsets

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

@article{cd349c25cb8441b482cc00fe99c793a1,
title = "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",
abstract = "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 Vβ5.2, Vβ8.1, Vβ8.1 + Vβ5.2, Vβ8.1(N), and Vβ8.1 were injected to the mice at dose of 200 μg/mouse. Vβ8.1 and Vβ5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-γ release, and prevented excessive IL-6, IL- 10, and TNF-α 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. Vβ8.1 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.",
author = "Bailin Liang and Zhen Zhang and Mohsen Araghiniknam and Cleamond Eskelson and Watson, {Ronald R}",
year = "1997",
month = "1",
language = "English (US)",
volume = "214",
pages = "87--94",
journal = "Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)",
issn = "0037-9727",
publisher = "Society for Experimental Biology and Medicine",
number = "1",

}

TY - JOUR

T1 - 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

AU - Liang, Bailin

AU - Zhang, Zhen

AU - Araghiniknam, Mohsen

AU - Eskelson, Cleamond

AU - Watson, Ronald R

PY - 1997/1

Y1 - 1997/1

N2 - 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 Vβ5.2, Vβ8.1, Vβ8.1 + Vβ5.2, Vβ8.1(N), and Vβ8.1 were injected to the mice at dose of 200 μg/mouse. Vβ8.1 and Vβ5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-γ release, and prevented excessive IL-6, IL- 10, and TNF-α 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. Vβ8.1 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.

AB - 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 Vβ5.2, Vβ8.1, Vβ8.1 + Vβ5.2, Vβ8.1(N), and Vβ8.1 were injected to the mice at dose of 200 μg/mouse. Vβ8.1 and Vβ5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-γ release, and prevented excessive IL-6, IL- 10, and TNF-α 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. Vβ8.1 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.

UR - http://www.scopus.com/inward/record.url?scp=0031025152&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031025152&partnerID=8YFLogxK

M3 - Article

VL - 214

SP - 87

EP - 94

JO - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)

JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)

SN - 0037-9727

IS - 1

ER -