Multiple mechanisms allow Mycobacterium tuberculosis to continuously inhibit MHC class II-mediated antigen presentation by macrophages. - Wikidata - awgldk - TriplyDB

Multiple mechanisms allow Mycobacterium tuberculosis to continuously inhibit MHC class II-mediated antigen presentation by macrophages.

Multiple mechanisms allow Mycobacterium tuberculosis to continuously inhibit MHC class II-mediated antigen presentation by macrophages.

http://www.wikidata.org/entity/Q33934507

about

Pathogenesis, immunology, and diagnosis of latent Mycobacterium tuberculosis infection Tuneable resolution as a systems biology approach for multi-scale, multi-compartment computational models Variability in tuberculosis granuloma T cell responses exists, but a balance of pro- and anti-inflammatory cytokines is associated with sterilization Identification of key processes that control tumor necrosis factor availability in a tuberculosis granuloma Both ligand- and cell-specific parameters control ligand agonism in a kinetic model of g protein-coupled receptor signaling.Exosomes derived from M. Bovis BCG infected macrophages activate antigen-specific CD4+ and CD8+ T cells in vitro and in vivo.Tuberculosis: global approaches to a global disease.New approaches in the diagnosis and treatment of latent tuberculosis infection The roles of immune memory and aging in protective immunity and endogenous reactivation of tuberculosis.Human cytomegalovirus decreases constitutive transcription of MHC class II genes in mature Langerhans cells by reducing CIITA transcript levels Virus infection rapidly activates the P58(IPK) pathway, delaying peak kinase activation to enhance viral replication.A Computational, Tissue-Realistic Model of Pressure Ulcer Formation in Individuals with Spinal Cord Injury.Systems biology approaches for understanding cellular mechanisms of immunity in lymph nodes during infection The Impaired Function of Macrophages Induced by Strenuous Exercise Could Not Be Ameliorated by BCAA Supplementation.Toward a multiscale model of antigen presentation in immunity.A hybrid multi-compartment model of granuloma formation and T cell priming in tuberculosis.Mathematical and computational approaches can complement experimental studies of host-pathogen interactions.Francisella tularensis induces ubiquitin-dependent major histocompatibility complex class II degradation in activated macrophages Immune Responses to Bacillus Calmette-Guérin Vaccination: Why Do They Fail to Protect against Mycobacterium tuberculosis?A multifaceted approach to modeling the immune response in tuberculosis.Function and Potentials of M. tuberculosis Epitopes Role of host- and pathogen-associated lipids in directing the immune response in mycobacterial infections, with emphasis on Mycobacterium avium subsp. paratuberculosis.Mycobacterial proteomics: analysis of expressed proteomes and post-translational modifications to identify candidate virulence factors.Immunoevasion and immunosuppression of the macrophage by Mycobacterium tuberculosis.Effect of multiple genetic polymorphisms on antigen presentation and susceptibility to Mycobacterium tuberculosis infection.Mouse Bone Marrow Sca-1+ CD44+ Mesenchymal Stem Cells Kill Avirulent Mycobacteria but Not Mycobacterium tuberculosis through Modulation of Cathelicidin Expression via the p38 Mitogen-Activated Protein Kinase-Dependent Pathway.Killer cell lectin-like receptor G1 deficiency significantly enhances survival after Mycobacterium tuberculosis infection.A comparison of random vs. chemotaxis-driven contacts of T cells with dendritic cells during repertoire scanning.Childhood tuberculosis is associated with decreased abundance of T cell gene transcripts and impaired T cell function.Mathematical Models for the Epidemiology and Evolution of Mycobacterium tuberculosis.Mycobacterium tuberculosis Exploits a Molecular Off Switch of the Immune System for Intracellular Survival.Rapid loss of early antigen-presenting activity of lymph node dendritic cells against Ag85A protein following Mycobacterium bovis BCG infection.

P2860

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P2860

Multiple mechanisms allow Mycobacterium tuberculosis to continuously inhibit MHC class II-mediated antigen presentation by macrophages.

http://www.wikidata.org/entity/Q33934507

description

2005 nî lūn-bûn

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2005 թուականի Մարտին հրատարակուած գիտական յօդուած

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2005 թվականի մարտին հրատարակված գիտական հոդված

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Multiple mechanisms allow Myco ...... n presentation by macrophages.

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Multiple mechanisms allow Myco ...... n presentation by macrophages.

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Multiple mechanisms allow Myco ...... n presentation by macrophages.

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Proceedings of the National Academy of Sciences of the United States of America

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Multiple mechanisms allow Myco ...... n presentation by macrophages.

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P2093

Denise E Kirschner

http://www.w3.org/2001/XMLSchema#string

Jennifer J Linderman

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Stewart T Chang

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P2860

Cell-mediated immunity: dealing a direct blow to pathogens.

Ligand-receptor interactions required for commitment to the activation of the interleukin 2 gene.

What is the role of nitric oxide in murine and human host defense against tuberculosis?Current knowledge.

Demonstration and partial characterization of the interferon-gamma receptor on human mononuclear phagocytes

The role of Toll-like receptors in immunity against mycobacterial infection.

Interaction of bacteria with antigen presenting cells: influences on antigen presentation and antibacterial immunity.

Virulence ranking of some Mycobacterium tuberculosis and Mycobacterium bovis strains according to their ability to multiply in the lungs, induce lung pathology, and cause mortality in mice.

MHC class II-derived peptides can bind to class II molecules, including self molecules, and prevent antigen presentation

Specificity and promiscuity among naturally processed peptides bound to HLA-DR alleles.

Major histocompatibility class I presentation of soluble antigen facilitated by Mycobacterium tuberculosis infection.

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4530-4535

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10.1073/PNAS.0500362102

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102

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Mycobacterium tuberculosis

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