Interferon γ eliminates responding CD4 T cells during mycobacterial infection by inducing apoptosis of activated CD4 T cells

Dyana K. Dalton, Laura Haynes, Cong Qiu Chu, Susan L. Swain, Susan Wittmer

Research output: Contribution to journalArticle

275 Scopus citations

Abstract

In Mycobacterium bovis Bacille Calmette-Guerin (BCG)-infected wild-type mice, there was a large expansion of an activated (CD44(hi)) splenic CD4 T cell population followed by a rapid contraction of this population to normal numbers. Contraction of the activated CD4 T cell population in wild-type mice was associated with increased apoptosis of activated CD4 T cells. In BCG- infected interferon (IFN)-γ knockout (KO) mice, the activated CD4 T cell population did not undergo apoptosis. These mice accumulated large numbers of CD4+CD44(hi) T cells that were responsive to mycobacterial antigens. Addition of IFN-γ to cultured splenocytes from BCG-infected IFN-γ KO mice induced apoptosis of activated CD4 T cells. IFN-γ-mediated apoptosis was abolished by depleting adherent cells or Mac-1+ spleen cells or by inhibiting nitric oxide synthase. Thus, IFN-γ is essential to a regulatory mechanism that eliminates activated CD4 T cells and maintains CD4 T cell homeostasis during an immune response.

Original languageEnglish (US)
Pages (from-to)117-122
Number of pages6
JournalJournal of Experimental Medicine
Volume192
Issue number1
DOIs
StatePublished - Jul 3 2000

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Keywords

  • Cell death
  • Homeostasis
  • Knockout mice
  • Nitric oxide
  • T lymphocytes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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