Essential pathogenetic role for interferon (IFN-)γ in concanavalin A-induced T cell-dependent hepatitis: Exacerbation by exogenous IFN-γ and prevention by IFN-γ receptor-immunoglobulin fusion protein

Ferdinando Nicoletti, Paola Zaccone, Ming Xiang, Gaetano Magro, Maurizio Di Mauro, Roberto Di Marco, Gianni Garotta, Pierluigi Meroni

Research output: Contribution to journalArticle

Abstract

We have studied the effects of either exogenously-administered interferon (IFN)-γ or of a nonimmunogenic mouse IFN-γ receptor-Immunoglobulin (IFN-γ R-Ig) fusion protein on the development of Concanavalin (Con)A-induced hepatitis in NMRI mice. PBS-treated control mice injected with 20 mg/kg ConA developed classical serological and histological signs of hepatitis with elevation of transaminases in the blood and infiltration of the liver by mononuclear cells and neutrophils. Treating the mice with rat IFN-γ 24 h prior to and 1 h after ConA-challenge markedly exacerbated these signs of hepatitis in a dose-dependent fashion. Moreover, mice injected with lower, non hepatitogenic, doses of ConA (10, 5 mg/kg) became fully susceptible to develop hepatitis upon similar treatment with IFN-γ. Concordantly, ConA-induced hepatitis was abrogated by either IFN-γ R-Ig fusion protein or anti-IFN-γ mAb. These data provide further evidence for the central pathogenetic role of endogenous IFN-γ in ConA-induced hepatitis and demonstrate the feasibility to prevent disease development by means of a non inmunogenic IFN-γ R-Ig fusion protein. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)315-323
Number of pages9
JournalCytokine
Volume12
Issue number4
DOIs
Publication statusPublished - Apr 2000

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Immunology
  • Immunology and Allergy

Fingerprint Dive into the research topics of 'Essential pathogenetic role for interferon (IFN-)γ in concanavalin A-induced T cell-dependent hepatitis: Exacerbation by exogenous IFN-γ and prevention by IFN-γ receptor-immunoglobulin fusion protein'. Together they form a unique fingerprint.

  • Cite this