Gamma interferon-mediated cytotoxicity related to murine Chlamydia trachomatis infection

G. I. Byrne, B. Grubbs, T. J. Marshall, J. Schachter, D. M. Williams

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


After infection with the mouse pneumonitis agent (MoPn; murine Chlamydia trachomatis), heterozygous (nu/+) but not nude athymic (nu/nu) mice produced enhanced amounts of gamma interferon (IFN-γ) in vitro in response to MoPn antigen that exhibited cytotoxic activity when added to host cells already infected with chlamydiae. Antibody-complement lysis showed the cytotoxic activity to be dependent, at least in part, on L3T4+ T cells for production. The cytotoxic responses were directed primarily against Chlamydia-infected target cells, but a second type of toxicity was demonstrable against uninfected target cells after treatment of the generating cell population with anti-Lyt-2 antibody plus complement at certain time points after infection. This additional nonspecific cytotoxic activity was presumably due to a second factor (factor X) acting in concert with IFN-γ. Lyt-2+ cells, however, also were shown to play a role in IFN-γ production and cytotoxicity directed against infected targets at later time points after infection. Neutralization of IFN-γ in the samples containing cytotoxic activity abrogated the cytotoxicity against both infected and uninfected targets, but cloned murine IFN-γ exhibited toxicity in a dose-dependent manner only against infected target cells. The data provides evidence that cytotoxicity against infected targets is due to antigen-specific induction of IFN-γ, but other cytokine activity, most demonstrable after removal of Lyt-2.2+ cells and cytotoxic to uninfected targets, also is present.

Original languageEnglish (US)
Pages (from-to)2023-2027
Number of pages5
JournalInfection and immunity
Issue number8
StatePublished - 1988
Externally publishedYes

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases


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