Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice

Jo Anne L. Flynn, Marsha M. Goldstein, John Chan, Karla J. Triebold, Klaus Pfeffer, Charles J. Lowenstein, Robert Schrelber, Tak W. Mak, Barry R. Bloom

Research output: Contribution to journalArticle

1278 Scopus citations

Abstract

Understanding the immunological mechanisms of protection and pathogenesis in tuberculosis remains problematic. We have examined the extent to which tumor necrosis factor-α (TNFα) contributes to this disease using murine models In which the action of TNFα is inhibited. TNFa was neutralized In vivo by monoclonal antibody; in addition, a mouse strain with a disruption in the gene for the 55 kDa TNF receptor was used. The data from both models established that TNFα and the 55 kDa TNF receptor are essential for protection against tuberculosis in mice, and for reactive nitrogen production by macrophages early in infection. Granulomas were formed in equal numbers in control and experimental mice, but necrosis was observed only in mice deficient in TNFα or TNF receptor. TNFα and the 55 kDa TNF receptor are necessary conditions for protection against murine M. tuberculosis infection, but are not solely responsible for the tissue damage observed.

Original languageEnglish (US)
Pages (from-to)561-572
Number of pages12
JournalImmunity
Volume2
Issue number6
DOIs
StatePublished - Jun 1995

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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    Flynn, J. A. L., Goldstein, M. M., Chan, J., Triebold, K. J., Pfeffer, K., Lowenstein, C. J., Schrelber, R., Mak, T. W., & Bloom, B. R. (1995). Tumor necrosis factor-α is required in the protective immune response against mycobacterium tuberculosis in mice. Immunity, 2(6), 561-572. https://doi.org/10.1016/1074-7613(95)90001-2