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

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

Research output: Contribution to journalArticlepeer-review

26 Scopus citations

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

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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