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Related Concept Videos

Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
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T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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The JAK-STAT Signaling Pathway

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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Related Experiment Video

Updated: May 14, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Meta-analysis demonstrates association between TLR polymorphisms and rheumatoid arthritis.

Y H Lee1, S-C Bae, G G Song

  • 1Division of Rheumatology, Department of Internal Medicine, College of Medicine, Korea University, Seoul, Korea. lyhcgh@korea.ac.kr

Genetics and Molecular Research : GMR
|February 20, 2013
PubMed
Summary

Toll-like receptor (TLR) gene variations may influence rheumatoid arthritis development and symptoms, particularly in Asian and Middle Eastern populations. Further research is needed to confirm these associations in diverse ethnic groups.

Related Experiment Videos

Last Updated: May 14, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Area of Science:

  • Immunogenetics
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease with complex etiology.
  • Genetic factors, including Toll-like receptor (TLR) polymorphisms, are implicated in RA susceptibility and progression.

Purpose of the Study:

  • To investigate the association between TLR polymorphisms and rheumatoid arthritis (RA) susceptibility.
  • To determine if TLR polymorphisms influence the clinical characteristics of RA.

Main Methods:

  • A meta-analysis was conducted on eleven studies involving 2078 RA patients and 2581 controls.
  • Studies were included if they provided at least two comparisons for a specific TLR polymorphism.
  • Data from European, Asian, and Middle Eastern populations were analyzed.

Main Results:

  • No significant association was found between TLR4 Asp299Gly (rs4986790) polymorphism and RA in European studies.
  • Significant associations were observed for TLR9 rs187084, TLR8 rs5741883, and TLR2 gene polymorphisms (GTn repeats) with RA in specific populations.
  • Overall meta-analysis indicated TLR polymorphism association with RA development and clinical features in Asian and Middle Eastern populations.

Conclusions:

  • TLR polymorphisms may play a role in the pathogenesis and clinical presentation of rheumatoid arthritis.
  • The association appears more pronounced in Asian and Middle Eastern populations compared to European populations.
  • Further investigation is warranted to elucidate the specific mechanisms and clinical implications of TLR polymorphisms in RA.