Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mesangial cells from patients with IgA nephropathy have increased susceptibility to galactose-deficient IgA1.

BMC nephrology - 5 Apr 2016

Ebefors Kerstin, Liu Peidi, Lassén Emelie, Elvin Johannes, Candemark Emma, Levan Kristina, Haraldsson Börje, Nyström Jenny

Abstract excerpt

BACKGROUND: IgA nephropathy (IgAN) is the most common glomerulonephritis in the world, affecting close to a million people. Circulating galactose-deficient IgA (gd-IgA), present in patients with IgAN, form immune complex deposits in the glomerular mesangium causing local proliferation and matrix expansion. Intriguing though, individuals having gd-IgA deposits in the kidneys do not necessarily have signs of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antigen-Antibody Complex
Share to Chemokine CCL5

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Galactose

Share to Glomerulonephritis, IGA

Share to Immunoglobulin A

Share to Immunologic Factors

Share to Interleukin-6

Share to Transforming Growth Factor beta1

Source

Open in PubMed Open full text

Identifiers

PMID: 27044423
DOI: 10.1186/s12882-016-0251-5
PMCID: PMC4820936

Genes

CCL5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mesangial cells from patients with IgA nephropathy have increased susceptibility to galactose-deficient IgA1.PMID 27044423Read ↗

The Pathophysiology of IgA NephropathySemantic proximity Read ↗

An update on the pathogenesis and treatment of IgA nephropathy.Semantic proximity Read ↗

Cellular signaling and production of galactose-deficient IgA1 in IgA nephropathy, an autoimmune disease.Semantic proximity Read ↗

IgA nephropathy.Semantic proximity Read ↗

Lessons from IgA Nephropathy ModelsSemantic proximity Read ↗

Pathogenesis of IgA nephropathy.Semantic proximity Read ↗

Transcriptomic and Proteomic Profiling Provides Insight into Mesangial Cell Function in IgA NephropathySemantic proximity Read ↗

Genetics and immunopathogenesis of IgA nephropathy.Semantic proximity Read ↗

Blood transcriptomic analysis reveals novel hub gene pathways associated with serum galactose-deficient IgA1 level in IgA nephropathySemantic proximity Read ↗

Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression of C1GALT1 and SP1 in plasmablast-like cell subpopulationsSemantic proximity Read ↗

Human IgA nephritis: immunocytochemical evidence of a chronic inflammatory proliferative disorder.Semantic proximity Read ↗

Phenotypic plasticity of mesenchymal stem cells is crucial for mesangial repair in a model of immunoglobulin light chain-associated mesangial damage.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.