Mechanism of cytolysis by lymphocytic choriomeningitis virus-specific, MHC class ii-restricted t-cells

A. J. Zaiac, D. G. Quinn, Jeffrey A Frelinger

Research output: Contribution to journalArticle

Abstract

β2-microglobulin deficient (βarrf) mice generate virusspecific, MHC class II restricted CD4+ CTL following infection with lymphocytic choriomeningitis virus (LCMV). The cytotoxic mechanisms employed by these CTL and the contribution of these effector functions to disease following virus infection was investigated. In standard 51Cr release assays lysis of infected target cells, by these virus specific CTL, is inhibited'by the presence of soluble FAS-lg fusion proteins. Furthermore, the cytolytic activity of the CD4+ CTL is ablated by the protein synthesis inhibitor emetine. These data indicate that these CTL utilize a FAS-dependent lytic mechanism. To investigate whether FAS expression is required for the development of disease following LCMV infection, β2m-.Ipr mice were infected with LCMV and monitored for morbidity and mortality. These FAS deficient mice succumbed to an illness which was similar to that seen in infected FAS expressing βjm" mice. Overall these studies suggest that cytotoxic effector function is not required for the development of LCM disease in βam- mice.

Original languageEnglish (US)
JournalFASEB Journal
Volume10
Issue number6
StatePublished - 1996
Externally publishedYes

Fingerprint

Lymphocytic choriomeningitis virus
cytolysis
Viruses
mice
Virus Diseases
cells
emetine
Emetine
infection
protein synthesis inhibitors
viruses
Protein Synthesis Inhibitors
morbidity
Assays
Fusion reactions
Morbidity
Mortality
assays
Infection
Proteins

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

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Mechanism of cytolysis by lymphocytic choriomeningitis virus-specific, MHC class ii-restricted t-cells. / Zaiac, A. J.; Quinn, D. G.; Frelinger, Jeffrey A.

In: FASEB Journal, Vol. 10, No. 6, 1996.

Research output: Contribution to journalArticle

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