T cell receptor Vβ complementarity-determining region 1 peptide administration moderates immune dysfunction and cytokine dysregulation induced by murine retrovirus infection

Ronald R Watson, J. Y. Wang, K. Dehghanpisheh, D. S. Huang, S. Wood, S. K. Ardestani, B. Liang, J. J. Marchalonis

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Murine AIDS, induced by LP-BM5 murine leukemia retrovirus infection, causes a progressive and profound immunodeficiency in female C57B1/6 mice. Previously, we reported that autoantibodies were elevated during the initiation phases of this murine retrovirus infection and bound peptide determinants corresponding to CDR1 of several TCR Vβ-chains. Therefore, we designed studies to determine whether administration of a major autoimmunogenic TCR Vβ CDR1 peptide before or after infection with LP-BM5 retrovirus would modulate retrovirus-induced dysregulation of T cell function. Administration of the TCR Vβ CDR1 peptide before murine retrovirus infection significantly prevented its suppression of splenic NK cell activity, T and B cell proliferation, and monokine (IL-6 and TNF-α) and Th1 cytokine (IL-2 and IFN-γ) release by splenocytes, and inhibited retrovirus- induced elevation of Th2 cytokine (IL-5 and IL-10). Similar data were obtained with peptide immunization 2 wk after murine retrovirus infection at 6 and 16 wk postinfection. However, delaying peptide immunization until severe suppression of T and B cell mitogenesis had occurred did not restore their functions. Immunization with TCR Vβ peptide prevents development of retrovirus-induced immune dysfunction, which suggests a possible pathogenic rope of autoreactive T cells as regulatory elements.

Original languageEnglish (US)
Pages (from-to)2282-2291
Number of pages10
JournalJournal of Immunology
Volume155
Issue number4
StatePublished - 1995

Fingerprint

Retroviridae Infections
Complementarity Determining Regions
Retroviridae
T-Cell Antigen Receptor
Cytokines
Immunization
Peptides
T-Lymphocytes
Murine Acquired Immunodeficiency Syndrome
B-Lymphocytes
Monokines
Interleukin-5
Regulatory T-Lymphocytes
Natural Killer Cells
Interleukin-10
Autoantibodies
Interleukin-2
Interleukin-6
Leukemia
Cell Proliferation

ASJC Scopus subject areas

  • Immunology

Cite this

T cell receptor Vβ complementarity-determining region 1 peptide administration moderates immune dysfunction and cytokine dysregulation induced by murine retrovirus infection. / Watson, Ronald R; Wang, J. Y.; Dehghanpisheh, K.; Huang, D. S.; Wood, S.; Ardestani, S. K.; Liang, B.; Marchalonis, J. J.

In: Journal of Immunology, Vol. 155, No. 4, 1995, p. 2282-2291.

Research output: Contribution to journalArticle

Watson, Ronald R ; Wang, J. Y. ; Dehghanpisheh, K. ; Huang, D. S. ; Wood, S. ; Ardestani, S. K. ; Liang, B. ; Marchalonis, J. J. / T cell receptor Vβ complementarity-determining region 1 peptide administration moderates immune dysfunction and cytokine dysregulation induced by murine retrovirus infection. In: Journal of Immunology. 1995 ; Vol. 155, No. 4. pp. 2282-2291.
@article{590a3802aeb642e38936fb205735c126,
title = "T cell receptor Vβ complementarity-determining region 1 peptide administration moderates immune dysfunction and cytokine dysregulation induced by murine retrovirus infection",
abstract = "Murine AIDS, induced by LP-BM5 murine leukemia retrovirus infection, causes a progressive and profound immunodeficiency in female C57B1/6 mice. Previously, we reported that autoantibodies were elevated during the initiation phases of this murine retrovirus infection and bound peptide determinants corresponding to CDR1 of several TCR Vβ-chains. Therefore, we designed studies to determine whether administration of a major autoimmunogenic TCR Vβ CDR1 peptide before or after infection with LP-BM5 retrovirus would modulate retrovirus-induced dysregulation of T cell function. Administration of the TCR Vβ CDR1 peptide before murine retrovirus infection significantly prevented its suppression of splenic NK cell activity, T and B cell proliferation, and monokine (IL-6 and TNF-α) and Th1 cytokine (IL-2 and IFN-γ) release by splenocytes, and inhibited retrovirus- induced elevation of Th2 cytokine (IL-5 and IL-10). Similar data were obtained with peptide immunization 2 wk after murine retrovirus infection at 6 and 16 wk postinfection. However, delaying peptide immunization until severe suppression of T and B cell mitogenesis had occurred did not restore their functions. Immunization with TCR Vβ peptide prevents development of retrovirus-induced immune dysfunction, which suggests a possible pathogenic rope of autoreactive T cells as regulatory elements.",
author = "Watson, {Ronald R} and Wang, {J. Y.} and K. Dehghanpisheh and Huang, {D. S.} and S. Wood and Ardestani, {S. K.} and B. Liang and Marchalonis, {J. J.}",
year = "1995",
language = "English (US)",
volume = "155",
pages = "2282--2291",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "4",

}

TY - JOUR

T1 - T cell receptor Vβ complementarity-determining region 1 peptide administration moderates immune dysfunction and cytokine dysregulation induced by murine retrovirus infection

AU - Watson, Ronald R

AU - Wang, J. Y.

AU - Dehghanpisheh, K.

AU - Huang, D. S.

AU - Wood, S.

AU - Ardestani, S. K.

AU - Liang, B.

AU - Marchalonis, J. J.

PY - 1995

Y1 - 1995

N2 - Murine AIDS, induced by LP-BM5 murine leukemia retrovirus infection, causes a progressive and profound immunodeficiency in female C57B1/6 mice. Previously, we reported that autoantibodies were elevated during the initiation phases of this murine retrovirus infection and bound peptide determinants corresponding to CDR1 of several TCR Vβ-chains. Therefore, we designed studies to determine whether administration of a major autoimmunogenic TCR Vβ CDR1 peptide before or after infection with LP-BM5 retrovirus would modulate retrovirus-induced dysregulation of T cell function. Administration of the TCR Vβ CDR1 peptide before murine retrovirus infection significantly prevented its suppression of splenic NK cell activity, T and B cell proliferation, and monokine (IL-6 and TNF-α) and Th1 cytokine (IL-2 and IFN-γ) release by splenocytes, and inhibited retrovirus- induced elevation of Th2 cytokine (IL-5 and IL-10). Similar data were obtained with peptide immunization 2 wk after murine retrovirus infection at 6 and 16 wk postinfection. However, delaying peptide immunization until severe suppression of T and B cell mitogenesis had occurred did not restore their functions. Immunization with TCR Vβ peptide prevents development of retrovirus-induced immune dysfunction, which suggests a possible pathogenic rope of autoreactive T cells as regulatory elements.

AB - Murine AIDS, induced by LP-BM5 murine leukemia retrovirus infection, causes a progressive and profound immunodeficiency in female C57B1/6 mice. Previously, we reported that autoantibodies were elevated during the initiation phases of this murine retrovirus infection and bound peptide determinants corresponding to CDR1 of several TCR Vβ-chains. Therefore, we designed studies to determine whether administration of a major autoimmunogenic TCR Vβ CDR1 peptide before or after infection with LP-BM5 retrovirus would modulate retrovirus-induced dysregulation of T cell function. Administration of the TCR Vβ CDR1 peptide before murine retrovirus infection significantly prevented its suppression of splenic NK cell activity, T and B cell proliferation, and monokine (IL-6 and TNF-α) and Th1 cytokine (IL-2 and IFN-γ) release by splenocytes, and inhibited retrovirus- induced elevation of Th2 cytokine (IL-5 and IL-10). Similar data were obtained with peptide immunization 2 wk after murine retrovirus infection at 6 and 16 wk postinfection. However, delaying peptide immunization until severe suppression of T and B cell mitogenesis had occurred did not restore their functions. Immunization with TCR Vβ peptide prevents development of retrovirus-induced immune dysfunction, which suggests a possible pathogenic rope of autoreactive T cells as regulatory elements.

UR - http://www.scopus.com/inward/record.url?scp=0029092656&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029092656&partnerID=8YFLogxK

M3 - Article

VL - 155

SP - 2282

EP - 2291

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 4

ER -