title: Autophagy as an immune effector against tuberculosis.
abstract: The now well-accepted innate immunity paradigm that autophagy acts as a cell-autonomous defense against intracellular bacteria has its key origins in studies with Mycobacterium tuberculosis, an important human pathogen and a model microorganism infecting macrophages. A number of different factors have been identified that play into the anti-mycobacterial functions of autophagy, and recent in vivo studies in the mouse model of tuberculosis have uncovered additional anti-inflammatory and tissue-sparing functions of autophagy. Complementing these observations, genome wide association studies indicate a considerable overlap between autophagy, human susceptibility to mycobacterial infections and predisposition loci for inflammatory bowel disease. Finally, recent studies show that autophagy is an important regulator and effector of IL-1 responses, and that autophagy intersects with type I interferon pathology-modulating responses.
authors.affiliation: Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
authors.forename: Steven B
authors.initials: SB
authors.lastname: Bradfute
authors.forename: Eliseo F
authors.initials: EF
authors.lastname: Castillo
authors.forename: John
authors.initials: J
authors.lastname: Arko-Mensah
authors.forename: Santosh
authors.initials: S
authors.lastname: Chauhan
authors.forename: Shanya
authors.initials: S
authors.lastname: Jiang
authors.forename: Michael
authors.initials: M
authors.lastname: Mandell
authors.forename: Vojo
authors.initials: V
authors.lastname: Deretic
mesh_terms: D000818:Animals; D001343:Autophagy; D004195:Disease Models, Animal; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D051379:Mice; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D014376:Tuberculosis / Q000276:immunology* / Q000382:microbiology*