Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling - Wikidata - wikimedia - TriplyDB

Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling

Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling

http://www.wikidata.org/entity/Q34083760

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Extrinsic and intrinsic control of macrophage inflammatory responses Immunometabolism in Tuberculosis IL-4Rα-dependent alternative activation of macrophages is not decisive for Mycobacterium tuberculosis pathology and bacterial burden in mice Antibodies trap tissue migrating helminth larvae and prevent tissue damage by driving IL-4Rα-independent alternative differentiation of macrophages Contribution of metabolic reprogramming to macrophage plasticity and function The E3 ubiquitin ligase neuregulin receptor degradation protein 1 (Nrdp1) promotes M2 macrophage polarization by ubiquitinating and activating transcription factor CCAAT/enhancer-binding Protein β (C/EBPβ)Macrophage polarization drives granuloma outcome during Mycobacterium tuberculosis infection Protective and pathogenic functions of macrophage subsets Microbial manipulation of receptor crosstalk in innate immunity Chitin activates parallel immune modules that direct distinct inflammatory responses via innate lymphoid type 2 and γδ T cells.Mycobacterium tuberculosis cell wall released fragments by the action of the human lung mucosa modulate macrophages to control infection in an IL-10-dependent manner Association of ESAT-6/CFP-10-induced IFN-γ, TNF-α and IL-10 with clinical tuberculosis: evidence from cohorts of pulmonary tuberculosis patients, household contacts and community controls in an endemic setting.Adventitial fibroblasts induce a distinct proinflammatory/profibrotic macrophage phenotype in pulmonary hypertension.Innate immune regulation by STAT-mediated transcriptional mechanisms.Progressive visceral leishmaniasis is driven by dominant parasite-induced STAT6 activation and STAT6-dependent host arginase 1 expression.Sleeping with the enemy: how intracellular pathogens cope with a macrophage lifestyle.Macrophage arginase-1 controls bacterial growth and pathology in hypoxic tuberculosis granulomas.Effect of apoptotic cell recognition on macrophage polarization and mycobacterial persistence.Obstacles and opportunities for understanding macrophage polarization.Differential and site specific impact of B cells in the protective immune response to Mycobacterium tuberculosis in the mouse.Role of arginase 1 from myeloid cells in th2-dominated lung inflammation.Interactome analysis of myeloid-derived suppressor cells in murine models of colon and breast cancer A Trypanosoma brucei kinesin heavy chain promotes parasite growth by triggering host arginase activity.A distal enhancer in Il12b is the target of transcriptional repression by the STAT3 pathway and requires the basic leucine zipper (B-ZIP) protein NFIL3.Type II cytokines impair host defense against an intracellular fungal pathogen by amplifying macrophage generation of IL-33.The pro-inflammatory cytokine, interleukin-6, enhances the polarization of alternatively activated macrophages.Preexisting helminth infection induces inhibition of innate pulmonary anti-tuberculosis defense by engaging the IL-4 receptor pathway.Adenosine promotes alternative macrophage activation via A2A and A2B receptors.GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury.Advanced age impairs macrophage polarization.In Situ Characterization of Splenic Brucella melitensis Reservoir Cells during the Chronic Phase of Infection in Susceptible Mice Expansion of myeloid-derived suppressor cells with arginase activity lasts longer in aged than in young mice after CpG-ODN plus IFA treatment.Quantifying crosstalk among interferon-γ, interleukin-12, and tumor necrosis factor signaling pathways within a TH1 cell model The tuberculous granuloma: an unsuccessful host defence mechanism providing a safety shelter for the bacteria?Platelet Supernatant Suppresses LPS-Induced Nitric Oxide Production from Macrophages Accompanied by Inhibition of NF-κB Signaling and Increased Arginase-1 Expression.Sustained generation of nitric oxide and control of mycobacterial infection requires argininosuccinate synthase 1.Genetic ablation of arginase 1 in macrophages and neutrophils enhances clearance of an arthritogenic alphavirus.Differential trafficking of TLR1 I602S underlies host protection against pathogenic mycobacteria.Interleukin-4- and interleukin-13-mediated alternatively activated macrophages: roles in homeostasis and disease.STAT3 regulates arginase-I in myeloid-derived suppressor cells from cancer patients.

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P2860

Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling

http://www.wikidata.org/entity/Q34083760

description

2010 nî lūn-bûn

@nan

2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2010年の論文

@ja

2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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type

label

Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Arginine usage in mycobacteria ...... e-paracrine cytokine signaling

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Amber M Smith

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Ashley A DeFreitas

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Geoffrey Neale

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Gilla Kaplan

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Huiyuan Zhang

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Mi-Sun Koo

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Peter J Murray

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P2860

Mechanism of inducible nitric oxide synthase exclusion from mycobacterial phagosomes

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells

Alternative activation of macrophages

Enhancer-mediated control of macrophage-specific arginase I expression

Regulation of immune responses by L-arginine metabolism

Nitric oxide and macrophage function

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

Nitric oxide and the immune response

Identification of nitric oxide synthase as a protective locus against tuberculosis

The role of the granuloma in expansion and dissemination of early tuberculous infection.

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