Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A. - Wikidata - wikimedia - TriplyDB

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

http://www.wikidata.org/entity/Q37591179

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Learning from myocarditis: mimicry, chaos and black holes Eosinophils in Autoimmune Diseases.Natural killer cells limit cardiac inflammation and fibrosis by halting eosinophil infiltration.P2×7 purinergic signaling in dilated cardiomyopathy induced by auto-immunity against muscarinic M2 receptors: autoantibody levels, heart functionality and cytokine expression.Cardiac myosin-Th17 responses promote heart failure in human myocarditis.Cannabidiol limits Tcell-mediated chronic autoimmune myocarditis: implications to autoimmune disorders and organ transplantation.Complexities in the relationship between infection and autoimmunity.Determinants of eosinophil survival and apoptotic cell death.Regulation of autoimmune myocarditis by host responses to the microbiome.Natural killer cells in inflammatory heart disease.Cardiac Autoimmunity: Myocarditis.Collaborative Interferon-γ and Interleukin-17 Signaling Protects the Oral Mucosa from Staphylococcus aureus Eosinophil-derived IL-4 drives progression of myocarditis to inflammatory dilated cardiomyopathy.Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart.Absence of nonhematopoietic MHC class II expression protects mice from experimental autoimmune myocarditis.Roles of Host Immunity in Viral Myocarditis and Dilated Cardiomyopathy.The Contribution of Autoantibodies to Inflammatory Cardiovascular Pathology.Viral myocarditis

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Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

http://www.wikidata.org/entity/Q37591179

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 18 September 2013

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

@en

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

@nl

type

label

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

@en

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

@nl

prefLabel

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

@en

Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A.

@nl

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JIMMUNOL.1301282

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Journal of Immunology

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Fatal eosinophilic myocarditis develops in the absence of IFN-γ and IL-17A

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Ashley B Cardamone

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DeLisa Fairweather

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Djahida Bedja

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Dongfeng Zheng

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G Christian Baldeviano

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Jobert G Barin

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Kathleen L Gabrielson

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Lei Wu

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Monica V Talor

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Noel R Rose

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P2860

Structure and signalling in the IL-17 receptor family

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Functional and pathogenic differences of Th1 and Th17 cells in experimental autoimmune encephalomyelitis

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

The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells

Multiple defects of immune cell function in mice with disrupted interferon-gamma genes

Interleukin-17 family members and inflammation

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

TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties

A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17

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10.4049/JIMMUNOL.1301282

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Daniela Cihakova

Jillian A Fontes

Natalie Stickel

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2013-09-18T00:00:00Z

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