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Related Experiment Videos

Interleukin 10 polymorphisms in ankylosing spondylitis.

V Goedecke1, A M Crane, E Jaakkola

  • 1WellcomeTrust Centre for Human Genetics, Roosevelt Drive, Headington, Oxfordm UK.

Genes and Immunity
|February 22, 2003
PubMed
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Interleukin-10 (IL10) promoter gene variations do not significantly impact susceptibility to ankylosing spondylitis (AS). However, specific IL10 polymorphisms may influence the age of disease onset and severity in AS patients.

Area of Science:

  • Genetics
  • Immunology
  • Rheumatology

Background:

  • Interleukin-10 (IL10) is a cytokine involved in immune regulation.
  • Genetic polymorphisms in the IL10 promoter region are associated with various autoimmune diseases.
  • Ankylosing spondylitis (AS) is a chronic inflammatory disease primarily affecting the spine.

Purpose of the Study:

  • To investigate the association between IL10 promoter polymorphisms and susceptibility to AS.
  • To examine the relationship between IL10 promoter polymorphisms and clinical manifestations of AS, including age of onset and disease severity.

Main Methods:

  • Studied three single nucleotide polymorphisms (SNPs: IL10-1087, -824, -597) and two microsatellites (IL10R, IL10G) in the IL10 promoter region.
  • Analyzed 468 individuals from 182 Finnish families with AS.

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  • Assessed associations with AS susceptibility, age of onset, and Bath Ankylosing Spondylitis Functional Index (BASFI).

    • Main Results:

    • No significant association was found between individual IL10 promoter polymorphisms or haplotypes and AS susceptibility.
    • A weak association was observed between IL10-597 and -824 SNPs and earlier age of disease onset (P=0.01 for each).
    • The IL10.G4 allele showed an association with BASFI, adjusted for disease duration (P=0.03).

    Conclusions:

    • IL10 promoter polymorphisms do not appear to significantly influence susceptibility to ankylosing spondylitis.
    • These genetic variations may play a minor role in determining the age of disease onset and functional severity in AS.