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A Method to Study the C924T Polymorphism of the Thromboxane A2 Receptor Gene
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TIRAP Ser180Leu polymorphism is associated with Behcet's disease.

Omar Durrani1, Katherine Banahan, Frederick J Sheedy

  • 1Academic Unit of Ophthalmology, School of Immunity and Infection, University of Birmingham, Vincent Drive, Birmingham B15 2TT, UK.

Rheumatology (Oxford, England)
|June 28, 2011
PubMed
Summary

This study investigated Toll-like receptors (TLRs) in Behçet's disease (BD). While TLR expression was similar across groups, a specific variant in TIRAP (TIR domain-containing adaptor protein) was linked to BD in UK patients.

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Area of Science:

  • Immunology
  • Genetics
  • Rheumatology

Background:

  • Behçet's disease (BD) etiology is unknown, with infection response suspected.
  • Toll-like receptors (TLRs) are crucial for mucosal immunity.
  • Single nucleotide polymorphisms (SNPs) in TLRs and associated genes were examined in BD.

Purpose of the Study:

  • To analyze SNPs in TLRs and related molecules in Behçet's disease patients.
  • To investigate the role of TLRs and associated genes in the pathogenesis of BD.
  • To determine if specific genetic variants are associated with BD susceptibility.

Main Methods:

  • Immunohistochemistry assessed TLR expression in buccal mucosa from BD patients, controls (lichen planus, pyogenic granuloma), and healthy individuals.
  • Single nucleotide polymorphism (SNP) analysis of CD14, TLR2, TLR4, and TIRAP (TIR domain-containing adaptor protein) was performed using SSP-PCR.
  • Patients were recruited from different geographical regions, including the UK and Middle East.

Main Results:

  • TLR expression was elevated in BD lesions but also in disease controls, indicating a general inflammatory response.
  • No significant association was found between BD and SNPs in CD14, TLR2, or TLR4.
  • A specific variant, TIRAP 180Leu, showed a significant association with BD in UK patients, but not in Middle Eastern patients.

Conclusions:

  • TLR expression levels in tissue did not differ significantly between BD patients and controls.
  • No differences in SNPs within TLR genes were observed compared to healthy controls.
  • The association of an increased function variant of TIRAP suggests a potential mechanism involving heightened cytokine production and tissue damage upon pathogen encounter at mucosal sites in BD.