Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis

Microbes Infect. 2011 Aug;13(8-9):749-56. doi: 10.1016/j.micinf.2011.03.002. Epub 2011 Mar 31.


Eicosanoids regulate whether human and murine macrophages infected with Mycobacterium tuberculosis die by apoptosis or necrosis. The death modality is important since apoptosis is associated with diminished pathogen viability and should be viewed as a form of innate immunity. Apoptotic vesicles derived from infected macrophages are also an important source of bacterial antigens that can be acquired by dendritic cells to prime antigen-specific T cells. This review integrates in vitro and in vivo data on how apoptosis of infected macrophages is linked to development of T cell immunity against M. tuberculosis.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • Eicosanoids / immunology*
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immunity, Cellular / immunology
  • Macrophages / immunology
  • Mice
  • Mycobacterium tuberculosis / immunology
  • Tuberculosis / immunology*


  • Eicosanoids