Increased Th17 cell frequency and poor clinical outcome in rheumatoid arthritis are associated with a genetic variant in the IL4R gene, rs1805010.

doi:10.1002/art.38343

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

Community

Back to search

Article

Increased Th17 cell frequency and poor clinical outcome in rheumatoid arthritis are associated with a genetic variant in the IL4R gene, rs1805010.

Arthritis & rheumatology (Hoboken, N.J.) - 1 May 2014

Leipe Jan, Schramm Markus A, Prots Iryna, Schulze-Koops Hendrik, Skapenko Alla

Abstract excerpt

OBJECTIVE: The minor allele of the IL4R gene single-nucleotide polymorphism, rs1805010, confers impaired interleukin-4 (IL-4) signaling and has been associated with an aggressive destructive course of rheumatoid arthritis (RA). IL-4 inhibits the development of Th17 cells, a cell population recently identified as being prominent in RA patients and being associated with cartilage and bone destruction. The purpose...

Read the complete abstract on PubMed

Topics

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

Share to Arthritis, Rheumatoid

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Interleukin-17

Share to Interleukin-22

Share to Interleukins

Share to Osteoarthritis

Share to Receptors, Interleukin-4

Share to Severity of Illness Index

Share to Th17 Cells

Source

Open in PubMed

Identifiers

PMID: 24782180
DOI: 10.1002/art.38343

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Increased Th17 cell frequency and poor clinical outcome in rheumatoid arthritis are associated with a genetic variant in the IL4R gene, rs1805010.PMID 24782180Read ↗

A polymorphism in the interleukin-4 receptor affects the ability of interleukin-4 to regulate Th17 cells: a possible immunoregulatory mechanism for genetic control of the severity of rheumatoid arthritis.Semantic proximity Read ↗

IL-4 polymorphisms (rs2227284, rs2243267, and rs2243270) are associated with reduced risk of rheumatoid arthritis.Semantic proximity Read ↗

Association of the IL4R single-nucleotide polymorphism I50V with rapidly erosive rheumatoid arthritis.Semantic proximity Read ↗

Association of interleukin-10 gene single nucleotide polymorphisms with rheumatoid arthritis in a Chinese population.Semantic proximity Read ↗

A functional variant of TLR10 modifies the activity of NFkB and may help predict a worse prognosis in patients with rheumatoid arthritis.Semantic proximity Read ↗

Pro-inflammatory cytokine response pre-dominates immuno-genetic pathway in development of rheumatoid arthritis.Semantic proximity Read ↗

Interleukin-17 and Toll-like Receptor 10 genetic polymorphisms and susceptibility to large joint osteoarthritis.Semantic proximity Read ↗

Interleukin10-1082 A/G polymorphism: Allele frequency, correlation with disease markers, messenger RNA and serum levels in North Indian rheumatoid arthritis patients.Semantic proximity Read ↗

Role of Th17 cells in human autoimmune arthritis.Semantic proximity Read ↗

Association of interleukin-4 receptor gene polymorphisms with rheumatoid arthritis in Egyptian female patients.Semantic proximity Read ↗

IL-4 VNTR gene polymorphism in chronic polyarthritis. The rare allele is associated with protection against destruction.Semantic proximity Read ↗

Associations of toll-like receptor (TLR)-4 single nucleotide polymorphisms and rheumatoid arthritis disease progression: an observational cohort study.Semantic proximity Read ↗

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