title: Human macrophage host defense against Mycobacterium tuberculosis.
abstract: Tuberculosis has plagued humans for ages, and understanding the host defense mechanisms against this pathogen has been a challenge to immunologists for decades. In mouse models of tuberculosis infection, the role of nitric oxide in antimicrobial activity is well defined. Recent studies indicate a role for the induction of autophagy in host defense against mycobacterial infection. In human macrophages, vitamin D-mediated induction of antimicrobial peptides appears to be an important player in combating Mycobacterium tuberculosis. Further understanding these defense mechanisms in human tuberculosis will help the development of new interventional strategies to prevent and treat disease.
authors.affiliation: Division of Dermatology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, United States. philip@bruinphd.com
authors.forename: Philip T
authors.initials: PT
authors.lastname: Liu
authors.forename: Robert L
authors.initials: RL
authors.lastname: Modlin
mesh_terms: D000818:Animals; D001343:Autophagy; D006801:Humans; D007113:Immunity, Innate; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D009569:Nitric Oxide / Q000378:metabolism; D053472:Nod Signaling Adaptor Proteins / Q000378:metabolism*; D051193:Toll-Like Receptors / Q000276:immunology* / Q000378:metabolism; D014376:Tuberculosis / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology; D014807:Vitamin D / Q000378:metabolism / Q000627:therapeutic use
chemical_list: D053472:Nod Signaling Adaptor Proteins; D051193:Toll-Like Receptors; D014807:Vitamin D; D009569:Nitric Oxide