IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice - Wikidata - awgldk - TriplyDB

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

http://www.wikidata.org/entity/Q37135557

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Study of Leishmania pathogenesis in mice: experimental considerations The influence of early neutrophil-Leishmania interactions on the host immune response to infection IL-22 Protects against Tissue Damage during Cutaneous Leishmaniasis IL-17 mediates immunopathology in the absence of IL-10 following Leishmania major infection Regulation of immunity during visceral Leishmania infection In vitro and in vivo efficacy of ether lipid edelfosine against Leishmania spp. and SbV-resistant parasites Pathogenesis of chagas' disease: parasite persistence and autoimmunity IL-4 attenuates Th1-associated chemokine expression and Th1 trafficking to inflamed tissues and limits pathogen clearance.Profiling of human acquired immunity against the salivary proteins of Phlebotomus papatasi reveals clusters of differential immunoreactivity.Systemic FasL and TRAIL neutralisation reduce leishmaniasis induced skin ulceration.Human dendritic cells exhibit a pronounced type I IFN signature following Leishmania major infection that is required for IL-12 induction A secondary wave of neutrophil infiltration causes necrosis and ulceration in lesions of experimental American cutaneous leishmaniasis IL-17 is essential for host defense against cutaneous Staphylococcus aureus infection in mice Keratinocytes determine Th1 immunity during early experimental leishmaniasis.BCG-mediated protection against Mycobacterium ulcerans infection in the mouse.Interleukin 1 (IL-1)- and IL-23-mediated expansion of filarial antigen-specific Th17 and Th22 cells in filarial lymphedema.Filaggrin-deficient mice exhibit TH17-dominated skin inflammation and permissiveness to epicutaneous sensitization with protein antigen The role of inflammatory, anti-inflammatory, and regulatory cytokines in patients infected with cutaneous leishmaniasis in Amazonas State, Brazil.Disease severity in patients infected with Leishmania mexicana relates to IL-1β.Evidence for involvement of Th17 type responses in post kala azar dermal leishmaniasis (PKDL).An early reduction in Treg cells correlates with enhanced local inflammation in cutaneous leishmaniasis in CCR6-deficient mice.Homeostatic tissue responses in skin biopsies from NOMID patients with constitutive overproduction of IL-1β.Leishmania major attenuates host immunity by stimulating local indoleamine 2,3-dioxygenase expression.IL-17 and Regulatory Cytokines (IL-10 and IL-27) in L. braziliensis Infection.Deletion of IL-4 receptor alpha on dendritic cells renders BALB/c mice hypersusceptible to Leishmania major infection.Key genomic changes necessary for an in vivo lethal mouse marburgvirus variant selection process.The involvement of TLR2 and TLR4 in cytokine and nitric oxide production in visceral leishmaniasis patients before and after treatment with anti-leishmanial drugs.An NLRP3 inflammasome-triggered Th2-biased adaptive immune response promotes leishmaniasis Enhanced production of IL-17A during zymosan-induced peritonitis in obese mice.Coinjection with TLR2 agonist Pam3CSK4 reduces the pathology of leishmanization in mice.Murine model of chronic L. (Viannia) panamensis infection: role of IL-13 in disease.Transcription of Toll-Like Receptors 2, 3, 4 and 9, FoxP3 and Th17 Cytokines in a Susceptible Experimental Model of Canine Leishmania infantum Infection.Does T Helper Differentiation Correlate with Resistance or Susceptibility to Infection with L. major? Some Insights From the Murine Model.T helper1/t helper2 cells and resistance/susceptibility to leishmania infection: is this paradigm still relevant?Protein biomarkers discriminate Leishmania major-infected and non-infected individuals in areas endemic for cutaneous leishmaniasis.Leishmaniavirus-Dependent Metastatic Leishmaniasis Is Prevented by Blocking IL-17A.Exosome Secretion by the Parasitic Protozoan Leishmania within the Sand Fly Midgut.IL-17A promotes susceptibility during experimental visceral leishmaniasis caused by Leishmania donovani Evaluation of recombinant Leishmania polyprotein plus glucopyranosyl lipid A stable emulsion vaccines against sand fly-transmitted Leishmania major in C57BL/6 mice Immunity to infection in IL-17-deficient mice and humans

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IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

http://www.wikidata.org/entity/Q37135557

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on March 2009

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

@en

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice.

@nl

type

label

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

@en

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice.

@nl

prefLabel

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

@en

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice.

@nl

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JIMMUNOL.0713598

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Journal of Immunology

P1476

IL-17 promotes progression of cutaneous leishmaniasis in susceptible mice

@en

P2093

Esther von Stebut

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Mark C Udey

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

Stephanie Dinges

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

Susanna Lopez Kostka

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

P2860

A receptor for the heterodimeric cytokine IL-23 is composed of IL-12Rbeta1 and a novel cytokine receptor subunit, IL-23R

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

Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17

STAT3 and NF-kappaB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice

Transforming growth factor-beta induces development of the T(H)17 lineage

TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells

Abnormal T cell activation caused by the imbalance of the IL-1/IL-1R antagonist system is responsible for the development of experimental autoimmune encephalomyelitis

Generation of large numbers of dendritic cells from mouse bone marrow cultures supplemented with granulocyte/macrophage colony-stimulating factor

IL-17 family cytokines and the expanding diversity of effector T cell lineages

Divergent roles of IL-23 and IL-12 in host defense against Klebsiella pneumoniae

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3039-3046

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scholarly article

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10.4049/JIMMUNOL.0713598

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5

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182

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Esther von Stebut

Susanna Lopez Kostka

Klaus G Griewank

Yoichiro Iwakura

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2009-03-01T00:00:00Z

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24032005

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19234200

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2658650

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