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Roles of Soluble and Membrane TNF and Related Ligands in Mycobacterial Infections: Effects of Selective and Non-selective TNF Inhibitors During Infection

  • Irene Garcia
  • Maria L. Olleros
  • Valerie F.J. Quesniaux
  • Muazzam Jacobs
  • Nasiema Allie
  • Sergei A. Nedospasov
  • David E. Szymkowski
  • Bernhard Ryffel
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 691)

Abstract

TNF plays an essential and non-redundant role in host defense mechanisms against Mycobacterium tuberculosis (Mtb) infection. TNF contributes to the development of granulomas, microstructures encasing pathogens and concentrating interactions between phagocytes and lymphocytes, and promotes bactericidal pathways to limit and destroy the invading intracellular pathogen. Production of TNF is associated with the development of human inflammatory diseases, and its inhibition, although an effective therapy, increases the risk of infections including either new or reactivation of tuberculosis infection. Studies on the role of membrane TNF in the absence of secreted TNF using genetic mouse models have shown that membrane TNF protects from M. bovis BCG and acute M. tuberculosis infections but does not induce inflammation in mouse. Pharmacological approaches of selective and non-selective soluble TNF inhibition show that a selective inhibitor of soluble TNF does not suppress host immunity to M. tuberculosis and M. bovis BCG infections, yet protects mice from arthritis and liver inflammatory diseases. This suggests that neutralization of soluble TNF may be effective to inhibit inflammatory diseases and also reduce the infection risks associated with current anti-TNF therapies.

Keywords

Tuberculosis Infection Mycobacterial Infection Latent Tuberculosis Bactericidal Mechanism Genetic Mouse Model 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Acknowledgment

This work was supported by grants from EC (TB REACT Contract no. 028190) and FNRS (to IG).

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© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Irene Garcia
    • 1
  • Maria L. Olleros
    • 1
  • Valerie F.J. Quesniaux
    • 2
  • Muazzam Jacobs
    • 3
  • Nasiema Allie
    • 3
  • Sergei A. Nedospasov
    • 4
    • 5
  • David E. Szymkowski
    • 6
  • Bernhard Ryffel
    • 7
  1. 1.Department of Pathology and ImmunologyCMU, University of GenevaGenevaSwitzerland
  2. 2.Orleans University and CNRS, Molecular Immunology and Embryology UMR6218OrleansFrance
  3. 3.Institute of Infectious Disease and Molecular Medicine, and National Health Laboratory ServiceUniversity of Cape TownCape TownSouth Africa
  4. 4.Laboratory of Molecular ImmunologyEngelhardt Institute of Molecular Biology, Russian Academy of SciencesMoscowRussia
  5. 5.German Rheumatism Research CenterBerlinGermany
  6. 6.Biotherapeutics Xencor, Inc.MonroviaUSA
  7. 7.Orleans University and CNRS, Molecular Immunology and EmbryologyOrleansFrance

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