title: Lipids, apoptosis, and cross-presentation: links in the chain of host defense against Mycobacterium tuberculosis.
abstract: 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.
authors: Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Smith Research Building, 1 Jimmy Fund Way, Boston, MA 02115, USA. sbehar@rics.bwh.harvard.edu
authors: Samuel M
authors: SM
authors: Behar
authors: Constance J
authors: CJ
authors: Martin
authors: Cláudio
authors: C
authors: Nunes-Alves
authors: Maziar
authors: M
authors: Divangahi
authors: Heinz G
authors: HG
authors: Remold
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D015777:Eicosanoids / Q000276:immunology*; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D009169:Mycobacterium tuberculosis / Q000276:immunology; D014376:Tuberculosis / Q000276:immunology*
chemical_list: D015777:Eicosanoids