Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy. - Wikidata - wikimedia - TriplyDB

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

http://www.wikidata.org/entity/Q35369982

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The Origin and Activities of IgA1-Containing Immune Complexes in IgA Nephropathy Recent advances in the understanding and management of IgA nephropathy New developments in the genetics, pathogenesis, and therapy of IgA nephropathy Genetic studies of IgA nephropathy: what have we learned from genome-wide association studies NF-κB in inflammation and renal diseases The microbiota and chronic kidney diseases: a double-edged sword Vibration Induces BAFF Overexpression and Aberrant O-Glycosylation of IgA1 in Cultured Human Tonsillar Mononuclear Cells in IgA Nephropathy.Differences in mouse and human nonmemory B cell pools.Microbiota and metabolome associated with immunoglobulin A nephropathy (IgAN).The genetics and immunobiology of IgA nephropathy.Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens.The development and survival but not function of follicular B cells is dependent on IL-7Rα Tyr449 signaling.Development of Animal Models of Human IgA Nephropathy Deficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infection Salivary Microbiota Associated with Immunoglobulin A Nephropathy.BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R Pathogenic Role of a Proliferation-Inducing Ligand (APRIL) in Murine IgA Nephropathy The kinase TBK1 controls IgA class switching by negatively regulating noncanonical NF-κB signaling.The Changing Landscape of Renal Inflammation Peyer's patches: organizing B-cell responses at the intestinal frontier Increased APRIL Expression Induces IgA1 Aberrant Glycosylation in IgA Nephropathy Matrix Producing Cells in Chronic Kidney Disease: Origin, Regulation, and Activation.Pathogenesis of immunoglobulin A nephropathy: recent insight from genetic studies.Association of systemic lupus erythematosus susceptibility genes with IgA nephropathy in a Chinese cohort IgA nephropathy and infections.New insights into the pathogenesis of IgA nephropathy: do toll like receptor 9-B cell activation factor-IgA class switching recombination signaling axis induce IgA hyper-production?Cellular signaling and production of galactose-deficient IgA1 in IgA nephropathy, an autoimmune disease.The intestine-renal connection in IgA nephropathy.Re-thinking the functions of IgA(+) plasma cells.The Role of TNF Superfamily Member 13 in the Progression of IgA Nephropathy.Emerging therapies in immunoglobulin A nephropathy.Targeting BAFF and APRIL in systemic lupus erythematosus and other antibody-associated diseases.Corticosteroids in IgA Nephropathy: Lessons from Recent Studies.The gut-kidney axis in IgA nephropathy: role of microbiota and diet on genetic predisposition.Biomarkers and targeted new therapies for IgA nephropathy.Toll-Like Receptor 9 Stimulation Induces Aberrant Expression of a Proliferation-Inducing Ligand by Tonsillar Germinal Center B Cells in IgA Nephropathy.Is there a role for immunosuppression in immunoglobulin A nephropathy?The non-canonical NF-κB pathway in immunity and inflammation.Update on immunoglobulin A nephropathy, Part I: Pathophysiology.Antibodies That Block or Activate Mouse B Cell Activating Factor of the Tumor Necrosis Factor (TNF) Family (BAFF), Respectively, Induce B Cell Depletion or B Cell Hyperplasia

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P2860

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

http://www.wikidata.org/entity/Q35369982

description

2011 nî lūn-bûn

@nan

2011 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

@zh-hk

2011年論文

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2011年論文

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2011年论文

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name

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@ast

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@en

type

label

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@ast

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@en

prefLabel

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@ast

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@en

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P1433

Journal of Clinical Investigation

P1476

Mice overexpressing BAFF develop a commensal flora-dependent, IgA-associated nephropathy.

@en

P2093

Adrian Papandile

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Andrew J Macpherson

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Ann Ranger

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Bruce A Julian

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Cheryl Wilson

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Douglas D McCarthy

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Elisa A Porfilio

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Jan Novak

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Jeannette Y Lee

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Julie Kujawa

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

P2860

The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88

Impaired IgA class switching in APRIL-deficient mice

The gut-joint axis: cross reactive food antibodies in rheumatoid arthritis

DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL

TACI is mutant in common variable immunodeficiency and IgA deficiency

Unravelling the pathogenesis of inflammatory bowel disease

Gut-residing segmented filamentous bacteria drive autoimmune arthritis via T helper 17 cells

Biased distribution of recombination sites within S regions upon immunoglobulin class switch recombination induced by transforming growth factor beta and lipopolysaccharide

Structural features of IgA molecules which contribute to IgA nephropathy.

Circulating immune complexes in IgA nephropathy consist of IgA1 with galactose-deficient hinge region and antiglycan antibodies

P304

3991-4002

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scholarly article

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10.1172/JCI45563

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P433

10

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121

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Jeffrey L. Browning

Jennifer L Gommerman

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2011-09-01T00:00:00Z

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51608901

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21881212

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3195458

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