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Rheumatoid arthritis.

D M Grennan, P A Sanders

    Bailliere'S Clinical Rheumatology
    |December 1, 1988
    PubMed
    Summary
    This summary is machine-generated.

    Genetic factors contribute to rheumatoid arthritis (RA) susceptibility, interacting with environmental triggers. Specific human leukocyte antigen (HLA) variants are linked to RA subgroups like Felty's syndrome and collagen-antibody positive RA.

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    Area of Science:

    • Immunogenetics
    • Rheumatology
    • Human Genetics

    Background:

    • Rheumatoid arthritis (RA) is understood to arise from genetic and environmental interactions.
    • Genetic predisposition to RA involves genes within the Major Histocompatibility Complex (MHC), notably HLA-DR4.
    • Specific MHC variants are associated with distinct RA subgroups.

    Purpose of the Study:

    • To investigate the genetic underpinnings of rheumatoid arthritis (RA) susceptibility.
    • To identify specific genetic markers associated with RA subgroups, including Felty's syndrome and collagen-antibody positive RA.
    • To explore the role of MHC and non-MHC genes in RA pathogenesis.

    Main Methods:

    • Analysis of family and twin studies to infer genetic contributions.
    • Examination of Human Leukocyte Antigen (HLA) and other Major Histocompatibility Complex (MHC) variants in RA patients.

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  • Investigation of associations with specific RA subgroups, such as Felty's syndrome and those with antibodies to native type II collagen.
  • Exploration of potential genetic loci on chromosome 14 and other candidate genes.

    • Main Results:

    • A strong association between HLA-DR4 and Felty's syndrome was observed.
    • DQ-beta and C4B null variants may indicate a haplotype linked to extra-articular disease in RA.
    • HLA-DR3 and HLA-DR7 showed associations with RA subgroups positive for antibodies to native type II collagen.
    • Gm associations differed between DR4-positive and collagen-antibody-positive RA subgroups.
    • Identified genetic markers account for only a portion of RA's genetic predisposition, suggesting additional loci are involved.

    Conclusions:

    • RA susceptibility results from oligogenic inheritance interacting with environmental factors.
    • Specific MHC and non-MHC genetic markers are associated with distinct RA phenotypes.
    • Multiple independent immunogenetic pathways, involving interactions at several loci, likely contribute to RA predisposition.