Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation - Wikidata - awgldk - TriplyDB

Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation

Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation

http://www.wikidata.org/entity/Q37143577

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Breakdown of Immune Tolerance in Systemic Lupus Erythematosus by Dendritic Cells Dendritic Cells in Systemic Lupus Erythematosus: From Pathogenic Players to Therapeutic Tools Emerging Role and Therapeutic Implication of Wnt Signaling Pathways in Autoimmune Diseases Caspase-8 acts as a molecular rheostat to limit RIPK1- and MyD88-mediated dendritic cell activation Requirement for MyD88 signaling in B cells and dendritic cells for germinal center anti-nuclear antibody production in Lyn-deficient mice Humanized TLR7/8 expression drives proliferative multisystemic histiocytosis in C57BL/6 mice.Complement opsonization of HIV-1 results in decreased antiviral and inflammatory responses in immature dendritic cells via CR3 The role of dendritic cells in tissue-specific autoimmunity.The role of tyrosine kinases in systemic lupus erythematosus and their potential as therapeutic targets.Innate immune programing by endotoxin and its pathological consequences Increased lung inflammation with oxygen supplementation in tracheotomized spontaneously breathing rabbits: an experimental prospective randomized study.The parasitic worm product ES-62 targets myeloid differentiation factor 88-dependent effector mechanisms to suppress antinuclear antibody production and proteinuria in MRL/lpr mice CD11c-mediated deletion of Flip promotes autoreactivity and inflammatory arthritis.Toll-like receptors: potential targets for lupus treatment LynA regulates an inflammation-sensitive signaling checkpoint in macrophages.Infectivity and insertional mutagenesis of endogenous retrovirus in autoimmune NZB and B/W mice.Neutrophils in animal models of autoimmune disease Immune Defense Protein Expression in Highly Purified Mouse Lung Epithelial Cells.T cells suppress memory-dependent rapid mucous cell metaplasia in mouse airways.LYN- and AIRE-mediated tolerance checkpoint defects synergize to trigger organ-specific autoimmunity.B cell-specific loss of Lyn kinase leads to autoimmunity Src family kinases Fyn and Lyn are constitutively activated and mediate plasmacytoid dendritic cell responses.Genetic dissection of dendritic cell homeostasis and function: lessons from cell type-specific gene ablation Self-antigen presentation by dendritic cells in autoimmunity.Functions of Murine Dendritic Cells.Deficiency in IRAK4 activity attenuates manifestations of murine Lupus.Spontaneous germinal centers and autoimmunity.Basophils contribute to pristane-induced Lupus-like nephritis model.Irgm1 coordinately regulates autoimmunity and host defense at select mucosal surfaces.Src family kinase tyrosine phosphorylates Toll-like receptor 4 to dissociate MyD88 and Mal/Tirap, suppressing LPS-induced inflammatory responses.Synergistic cooperation and crosstalk between MYD88L265P and mutations that dysregulate CD79B and surface IgM.Transcriptional determinants of individualized inflammatory responses at anatomically separate sites.Toll-like receptors in lupus nephritis.Lyn, Lupus, and (B) Lymphocytes, a Lesson on the Critical Balance of Kinase Signaling in Immunity.Multilayer Control of B Cell Activation by the B Cell Antigen Receptor: Following Themes Initiated With Bill Paul.

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Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation

http://www.wikidata.org/entity/Q37143577

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 12 August 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Hyperactivated MyD88 signaling ...... autoimmunity and inflammation

@en

Hyperactivated MyD88 signaling ...... autoimmunity and inflammation.

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type

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Hyperactivated MyD88 signaling ...... autoimmunity and inflammation

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Hyperactivated MyD88 signaling ...... autoimmunity and inflammation.

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Hyperactivated MyD88 signaling ...... autoimmunity and inflammation

@en

Hyperactivated MyD88 signaling ...... autoimmunity and inflammation.

@nl

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PNAS.1300617110

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

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Hyperactivated MyD88 signaling ...... autoimmunity and inflammation

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Anthony L DeFranco

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

Chrystelle Lamagna

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

Clifford A Lowell

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

Jessica A van Ziffle

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

Patrizia Scapini

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

P2860

Dynamic regulation of neutrophil survival through tyrosine phosphorylation or dephosphorylation of caspase-8

Constitutive ablation of dendritic cells breaks self-tolerance of CD4 T cells and results in spontaneous fatal autoimmunity

Activation of murine macrophages via TLR2 and TLR4 is negatively regulated by a Lyn/PI3K module and promoted by SHIP1

The Lyn tyrosine kinase differentially regulates dendritic cell generation and maturation

Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

Developmental acquisition of the Lyn-CD22-SHP-1 inhibitory pathway promotes B cell tolerance

Toll-like receptors activate innate and adaptive immunity by using dendritic cell-intrinsic and -extrinsic mechanisms

Interleukin 10 acts on regulatory T cells to maintain expression of the transcription factor Foxp3 and suppressive function in mice with colitis

Myeloid cells, BAFF, and IFN-gamma establish an inflammatory loop that exacerbates autoimmunity in Lyn-deficient mice.

Dendritic cells in lupus are not required for activation of T and B cells but promote their expansion, resulting in tissue damage

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E3311-20

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scholarly article

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10.1073/PNAS.1300617110

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35

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2013-08-12T00:00:00Z

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23940344

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