Scientific article

TNF in host resistance to tuberculosis infection

Published inCurrent directions in autoimmunity, vol. 11, p. 157-179
Publication date2010

TNF is essential to control Mycobacterium tuberculosis infection and cannot be replaced by other proinflammatory cytokines. Overproduction of TNF may cause immunopathology, while defective TNF production results in uncontrolled infection. The critical role of TNF in the control of tuberculosis has been illustrated recently by primary and reactivation of latent infection in some patients under pharmacological anti-TNF therapy for rheumatoid arthritis or Crohn's disease. In this review, we discuss results of recent studies aimed at better understanding of molecular, cellular and kinetic aspects of TNF-mediated regulation of host-mycobacteria interactions. In particular, recent data using either mutant mice expressing solely membrane TNF or specific inhibitor sparing membrane TNF demonstrated that membrane TNF is sufficient to control acute M. tuberculosis infection. This is opening the way to selective TNF neutralization that might retain the desired anti-inflammatory effect but reduce the infectious risk.

  • Animals
  • Antibodies, Neutralizing/adverse effects
  • Host-Pathogen Interactions/*immunology
  • Humans
  • Inflammation/immunology
  • Lymphocyte Activation
  • Macrophage Activation
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Models, Immunological
  • Mycobacterium tuberculosis/immunology
  • T-Lymphocytes/immunology
  • Tuberculosis/*immunology
  • Tumor Necrosis Factor-alpha/deficiency/genetics/*immunology
Citation (ISO format)
QUESNIAUX, Valerie F. J. et al. TNF in host resistance to tuberculosis infection. In: Current directions in autoimmunity, 2010, vol. 11, p. 157–179. doi: 10.1159/000289204
ISSN of the journal1422-2132

Technical informations

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