C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes. - Wikidata - wikimedia - TriplyDB

C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes.

C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes.

http://www.wikidata.org/entity/Q34729450

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Breakdown of Immune Tolerance in Systemic Lupus Erythematosus by Dendritic Cells SLE-associated risk factors affect DC function TLRs and interferons: a central paradigm in autoimmunity Cause and consequences of the activated type I interferon system in SLE Tartrate-resistant acid phosphatase deficiency causes a bone dysplasia with autoimmunity and a type I interferon expression signature.Blood gene expression profiling in pediatric systemic lupus erythematosus and systemic juvenile idiopathic arthritis: from bench to bedside.Evidence for C1q-mediated crosslinking of CD33/LAIR-1 inhibitory immunoreceptors and biological control of CD33/LAIR-1 expression.C1 Complex: An Adaptable Proteolytic Module for Complement and Non-Complement Functions Monocyte differentiation and macrophage priming are regulated differentially by pentraxins and their ligands Complement C4 maintains peripheral B-cell tolerance in a myeloid cell dependent manner.Pivotal Functions of Plasmacytoid Dendritic Cells in Systemic Autoimmune Pathogenesis.The inflammasome and lupus: another innate immune mechanism contributing to disease pathogenesis?Do follicular dendritic cells regulate lupus-specific B cells?Type I interferons are associated with subclinical markers of cardiovascular disease in a cohort of systemic lupus erythematosus patients.Aicardi-Goutières syndrome and the type I interferonopathies.Requirements for innate immune pathways in environmentally induced autoimmunity.C1q-mediated repression of human monocytes is regulated by leukocyte-associated Ig-like receptor 1 (LAIR-1).The type I interferon system in the etiopathogenesis of autoimmune diseases.Type I interferon and systemic lupus erythematosus.Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.Complement protein C1q directs macrophage polarization and limits inflammasome activity during the uptake of apoptotic cells.C1q protein binds to the apoptotic nucleolus and causes C1 protease degradation of nucleolar proteins.C1q limits dendritic cell differentiation and activation by engaging LAIR-1 Genetics of SLE: functional relevance for monocytes/macrophages in disease Neutrophil extracellular trap-associated protein activation of the NLRP3 inflammasome is enhanced in lupus macrophages C1q Modulates the Response to TLR7 Stimulation by Pristane-Primed Macrophages: Implications for Pristane-Induced Lupus.Uncoupling complement C1s activation from C1q binding in apoptotic cell phagocytosis and immunosuppressive capacity.C-reactive protein inhibits plasmacytoid dendritic cell interferon responses to autoantibody immune complexes Proteolytic inactivation of nuclear alarmin high-mobility group box 1 by complement protease C1s during apoptosis Anti-DNA antibodies cross-react with C1q Type I interferon-mediated monogenic autoinflammation: The type I interferonopathies, a conceptual overview Fueling autoimmunity: type I interferon in autoimmune diseases.The identification of a novel splicing mutation in C1qB in a Japanese family with C1q deficiency: a case report.Assessment of Type I Interferon Signaling in Pediatric Inflammatory Disease.Disease mechanisms in rheumatology--tools and pathways: plasmacytoid dendritic cells and their role in autoimmune rheumatic diseases.Possible novel biomarkers of organ involvement in systemic lupus erythematosus.Beyond apoptosis in lupus.Complement, c1q, and c1q-related molecules regulate macrophage polarization.Systemic Lupus Erythematosus--A Disease with A Dysregulated Type I Interferon System.Insights from Mendelian Interferonopathies: Comparison of CANDLE, SAVI with AGS, Monogenic Lupus.

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C1q deficiency leads to the defective suppression of IFN-alpha in response to nucleoprotein containing immune complexes.

http://www.wikidata.org/entity/Q34729450

description

2010 nî lūn-bûn

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2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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JIMMUNOL.1001731

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Journal of Immunology

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Brian E Hall

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Chih Long Liu

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Deanna M Santer

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Keith B Elkon

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Stephanie Tangsombatvisit

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Thaddeus C George

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P2860

Regulation of TLR7/9 responses in plasmacytoid dendritic cells by BST2 and ILT7 receptor interaction

gC1q receptor ligation selectively down-regulates human IL-12 production through activation of the phosphoinositide 3-kinase pathway

Cross-regulation of TNF and IFN-alpha in autoimmune diseases

BDCA-2, a novel plasmacytoid dendritic cell-specific type II C-type lectin, mediates antigen capture and is a potent inhibitor of interferon alpha/beta induction

Complement. Second of two parts

Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus

Methods for the separation, purification and measurement of nine components of hemolytic complement in guinea-pig serum

The 1982 revised criteria for the classification of systemic lupus erythematosus

Interferon and granulopoiesis signatures in systemic lupus erythematosus blood

Tolerogenic dendritic cells

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4738-4749

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scholarly article

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10.4049/JIMMUNOL.1001731

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8

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185

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Peter D Arkwright

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2010-09-15T00:00:00Z

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46281559

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20844193

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3065655

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