title: Insights into battles between Mycobacterium tuberculosis and macrophages.
abstract: As the first line of immune defense for Mycobacterium tuberculosis (Mtb), macrophages also provide a major habitat for Mtb to reside in the host for years. The battles between Mtb and macrophages have been constant since ancient times. Triggered upon Mtb infection, multiple cellular pathways in macrophages are activated to initiate a tailored immune response toward the invading pathogen and regulate the cellular fates of the host as well. Toll-like receptors (TLRs) expressed on macrophages can recognize pathogen-associated-molecular patterns (PAMPs) on Mtb and mediate the production of immune-regulatory cytokines such as tumor necrosis factor (TNF) and type I Interferons (IFNs). In addition, Vitamin D receptor (VDR) and Vitamin D-1-hydroxylase are up-regulated in Mtb-infected macrophages, by which Vitamin D participates in innate immune responses. The signaling pathways that involve TNF, type I IFNs and Vitamin D are inter-connected, which play critical roles in the regulation of necroptosis, apoptosis, and autophagy of the infected macrophages. This review article summarizes current knowledge about the interactions between Mtb and macrophages, focusing on cellular fates of the Mtb-infected macrophages and the regulatory molecules and cellular pathways involved in those processes.
authors.affiliation: CAS key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.
authors.forename: Guanghua
authors.initials: G
authors.lastname: Xu
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: George Fu
authors.initials: GF
authors.lastname: Gao
authors.forename: Cui Hua
authors.initials: CH
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis; D001343:Autophagy; D006801:Humans; D007370:Interferon Type I / Q000378:metabolism; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D009169:Mycobacterium tuberculosis / Q000502:physiology*; D018167:Receptors, Calcitriol / Q000378:metabolism; D013250:Steroid Hydroxylases / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism; D014376:Tuberculosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D048069:Tumor Necrosis Factors / Q000378:metabolism
chemical_list: D007370:Interferon Type I; D018167:Receptors, Calcitriol; D051193:Toll-Like Receptors; D048069:Tumor Necrosis Factors; D013250:Steroid Hydroxylases; C406322:vitamin D 1-alpha hydroxylase