Cell death and autophagy in tuberculosis

Semin Immunol. 2014 Dec;26(6):497-511. doi: 10.1016/j.smim.2014.10.001. Epub 2014 Oct 17.

Abstract

Mycobacterium tuberculosis has succeeded in infecting one-third of the human race though inhibition or evasion of innate and adaptive immunity. The pathogen is a facultative intracellular parasite that uses the niche provided by mononuclear phagocytes for its advantage. Complex interactions determine whether the bacillus will or will not be delivered to acidified lysosomes, whether the host phagocyte will survive infection or die, and whether the timing and mode of cell death works to the advantage of the host or the pathogen. Here we discuss cell death and autophagy in TB. These fundamental processes of cell biology feature in all aspects of TB pathogenesis and may be exploited to the treatment or prevention of TB disease.

Keywords: Apoptosis; Autophagy; Necrosis; Phagocyte; Tuberculosis.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Apoptosis / immunology*
  • Apoptosis Regulatory Proteins / genetics
  • Apoptosis Regulatory Proteins / immunology
  • Autophagy / immunology*
  • Bacterial Proteins / genetics
  • Bacterial Proteins / immunology
  • Gene Expression Regulation
  • Humans
  • Immune Evasion*
  • Immunity, Innate
  • Macrophages / immunology*
  • Macrophages / microbiology
  • Macrophages / pathology
  • Mycobacterium tuberculosis / immunology*
  • Necrosis / genetics
  • Necrosis / immunology
  • Necrosis / microbiology
  • Necrosis / pathology
  • Perforin / genetics
  • Perforin / immunology
  • Phagosomes / immunology
  • Phagosomes / microbiology
  • Phagosomes / pathology
  • Signal Transduction
  • Tuberculosis, Pulmonary / genetics
  • Tuberculosis, Pulmonary / immunology*
  • Tuberculosis, Pulmonary / microbiology
  • Tuberculosis, Pulmonary / pathology

Substances

  • Apoptosis Regulatory Proteins
  • Bacterial Proteins
  • Perforin