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HLA-DQA1*0501 is associated with diffuse systemic sclerosis in Caucasian men

N C Lambert1, O Distler, U Müller-Ladner

  • 1Immunogenetics Program, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA.

Arthritis and Rheumatism
|October 3, 2000
PubMed

Insights

A specific Human Leukocyte Antigen (HLA) DQA1 allele is linked to systemic sclerosis (SSc) in men, suggesting a greater genetic contribution of HLA genes to SSc risk in males. This finding advances understanding of SSc pathogenesis in men.

Area of Science:

  • Immunogenetics
  • Rheumatology
  • Human Genetics

Background:

  • Systemic sclerosis (SSc) is a rare autoimmune disease with limited understanding of its pathogenesis in men.
  • Human Leukocyte Antigen (HLA) class II alleles are implicated in autoimmune diseases, but their specific role in male SSc is underexplored.

Purpose of the Study:

  • To investigate HLA class II alleles (DQA1, DQB1, DRB1) in Caucasian men with SSc.
  • To explore the hypothesis that maternal HLA compatibility is a risk factor for SSc in men.

Main Methods:

  • Sequence-specific oligonucleotide probe typing was employed to determine HLA DQA1, DQB1, and DRB1 alleles.
  • Allele frequencies were compared between SSc patients (50 men, 36 parous women) and healthy controls (59 men, 80 parous women).
  • Mothers of SSc patients and healthy men were also genotyped to assess maternal HLA compatibility.

Main Results:

  • The DQA1*0501 allele was significantly more frequent in men with SSc compared to healthy men (OR 2.3, P=0.006).
  • DQA1*0501 was specifically associated with diffuse SSc in men (OR 3.0, P=0.004).
  • No increased risk of SSc in men was associated with maternal HLA compatibility.

Conclusions:

  • A specific DQA1 allele (DQA1*0501) is associated with SSc in men, potentially explaining previously observed DRB1 associations due to linkage disequilibrium.
  • The genetic contribution of HLA genes to SSc risk appears substantially greater in men than in parous women.
  • This study highlights sex-specific genetic factors in SSc pathogenesis.
Abstract

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