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[Contribution of non-HLA genes to juvenile idiopathic arthritis susceptibility]

K V Savost'anov, E I Alexeeva, D A Chistiakov

    Vestnik Rossiiskoi Akademii Meditsinskikh Nauk
    |March 31, 2015
    PubMed

    Insights

    Juvenile idiopathic arthritis (JIA) is a common childhood joint inflammation disorder. Genetic factors, including HLA and non-HLA regions, significantly contribute to JIA susceptibility and may share pathways with adult rheumatoid arthritis.

    Area of Science:

    • Rheumatology
    • Genetics
    • Immunology

    Context:

    • Juvenile idiopathic arthritis (JIA) is the most prevalent chronic rheumatologic condition in pediatric populations.
    • Chronic joint inflammation is the hallmark clinical presentation of JIA, a complex group of disorders.
    • The Human Leukocyte Antigen (HLA) region is a primary genetic susceptibility locus for JIA, accounting for approximately 17% of familial disease segregation.

    Purpose:

    • To review the genetic architecture of Juvenile idiopathic arthritis (JIA).
    • To highlight the role of both HLA and non-HLA genetic loci in JIA pathogenesis.
    • To explore potential shared mechanisms between JIA and adult rheumatoid arthritis.

    Summary:

    • Genome-wide association studies and meta-analyses have identified over 20 non-HLA susceptibility loci for JIA.
    • A significant portion of these non-HLA loci are also implicated in rheumatoid arthritis, suggesting conserved pathogenic pathways.
    • Emerging evidence points towards a potential role for epigenetic modifications in JIA development, warranting further investigation.

    Impact:

    • Understanding the genetic basis of JIA can inform diagnostic strategies and therapeutic targets.
    • Identifying shared genetic factors with rheumatoid arthritis may lead to novel treatment approaches for both conditions.
    • Future research into epigenetic alterations could uncover new avenues for JIA prevention and management.

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