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Interferon gamma activated macrophages kill mycobacteria by nitric oxide induced apoptosis

Interferon gamma activated macrophages kill mycobacteria by nitric oxide induced apoptosis

http://www.wikidata.org/entity/Q28478015

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The Case for Live Attenuated Vaccines against the Neglected Zoonotic Diseases Brucellosis and Bovine Tuberculosis A Simple, Reproducible, Inexpensive, Yet Old-Fashioned Method for Determining Phagocytic and Bactericidal Activities of Macrophages Important Role of the IL-32 Inflammatory Network in the Host Response against Viral Infection Differential effects of type I and II interferons on myeloid cells and resistance to intracellular bacterial infections Versatile myeloid cell subsets contribute to tuberculosis-associated inflammation Striking the Right Balance Determines TB or Not TB Non-Canonical Cell Death Induced by p53 Plasmodium cellular effector mechanisms and the hepatic microenvironment Proteomic Analysis of Drug-Resistant Mycobacteria: Co-Evolution of Copper and INH Resistance G1-4A, a Polysaccharide from Tinospora cordifolia Inhibits the Survival of Mycobacterium tuberculosis by Modulating Host Immune Responses in TLR4 Dependent Manner The M1 and M2 paradigm of macrophage activation: time for reassessment Genome-wide transcriptional profiling of peripheral blood leukocytes from cattle infected with Mycobacterium bovis reveals suppression of host immune genes.Networked T cell death following macrophage infection by Mycobacterium tuberculosis.Attenuated Mycobacterium tuberculosis SO2 vaccine candidate is unable to induce cell death.Natural transmission of Plasmodium berghei exacerbates chronic tuberculosis in an experimental co-infection model Characterizing virulence-specific perturbations in the mitochondrial function of macrophages infected with Mycobacterium tuberculosis.MicroRNA-155 promotes autophagy to eliminate intracellular mycobacteria by targeting Rheb Macrophage immunoregulatory pathways in tuberculosis.YopP-expressing variant of Y. pestis activates a potent innate immune response affording cross-protection against yersiniosis and tularemia [corrected].Infection of human monocytes by Chlamydia pneumoniae and Chlamydia trachomatis: an in vitro comparative study Interactions between naïve and infected macrophages reduce Mycobacterium tuberculosis viability Lipid metabolism and Type VII secretion systems dominate the genome scale virulence profile of Mycobacterium tuberculosis in human dendritic cells.Mycobacterium leprae-Infected Macrophages Preferentially Primed Regulatory T Cell Responses and Was Associated with Lepromatous Leprosy.Interferon-γ Is a Crucial Activator of Early Host Immune Defense against Mycobacterium ulcerans Infection in Mice.Investigating the Role of TNF-α and IFN-γ Activation on the Dynamics of iNOS Gene Expression in LPS Stimulated Macrophages Trehalose dimycolate interferes with FcγR-mediated phagosome maturation through Mincle, SHP-1 and FcγRIIB signalling.IFN-γ-mediated hematopoietic cell destruction in murine models of immune-mediated bone marrow failure.IFN-γ fails to overcome inhibition of selected macrophage activation events in response to pathogenic mycobacteria Differential trafficking of TLR1 I602S underlies host protection against pathogenic mycobacteria.Autophagy hijacked through viroporin-activated calcium/calmodulin-dependent kinase kinase-β signaling is required for rotavirus replication One Episode of Self-Resolving Plasmodium yoelii Infection Transiently Exacerbates Chronic Mycobacterium tuberculosis Infection.Molecular immunologic correlates of spontaneous latency in a rabbit model of pulmonary tuberculosis.Insufficient Generation of Mycobactericidal Mediators and Inadequate Level of Phagosomal Maturation Are Related with Susceptibility to Virulent Mycobacterium tuberculosis Infection in Mouse Macrophages.Mycobacterium tuberculosis exploits human interferon γ to stimulate macrophage extracellular trap formation and necrosis.Dipterinyl calcium pentahydrate inhibits intracellular mycobacterial growth in human monocytes via the C-C chemokine MIP-1β and nitric oxide.Leishmania-encoded orthologs of macrophage migration inhibitory factor regulate host immunity to promote parasite persistence.Mycobacterium leprae-induced Insulin-like Growth Factor I attenuates antimicrobial mechanisms, promoting bacterial survival in macrophages.Persistence of the bacterial pathogen Granulibacter bethesdensis in chronic granulomatous disease monocytes and macrophages lacking a functional NADPH oxidase.Role of Cathepsins in Mycobacterium tuberculosis Survival in Human Macrophages.Truncated hemoglobin, HbN, is post-translationally modified in Mycobacterium tuberculosis and modulates host-pathogen interactions during intracellular infection.

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Interferon gamma activated macrophages kill mycobacteria by nitric oxide induced apoptosis

http://www.wikidata.org/entity/Q28478015

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2011 nî lūn-bûn

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2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2011 թվականի մայիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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name

Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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type

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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Interferon gamma activated mac ...... nitric oxide induced apoptosis

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P2860

LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

The Role of Nitric Oxide in Mycobacterial Infections

Apoptosis: a review of programmed cell death

Strains of Mycobacterium tuberculosis differ in susceptibility to reactive nitrogen intermediates in vitro

Susceptibility of a panel of virulent strains of Mycobacterium tuberculosis to reactive nitrogen intermediates

Methods in mammalian autophagy research

Autophagy is a defense mechanism inhibiting BCG and Mycobacterium tuberculosis survival in infected macrophages

Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages

Identification of nitric oxide synthase as a protective locus against tuberculosis

Virulent Mycobacterium tuberculosis strains evade apoptosis of infected alveolar macrophages.

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