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The complement components coded in the major histocompatibility complexes and their biological activities.

R R Porter

    Immunological Reviews
    |October 1, 1985
    PubMed
    Summary
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    The complement system involves two pathways regulated by control proteins. Genetic variations in complement components C2, factor B, and C4 within the MHC influence autoimmune disease susceptibility.

    Area of Science:

    • Immunology
    • Genetics
    • Molecular Biology

    Background:

    • The complement system comprises two proteolytic cascade pathways with shared components and regulatory proteins.
    • Key complement components (C2, factor B, C4) are encoded by genes located within the Major Histocompatibility Complex (MHC).
    • These MHC-linked genes exhibit significant polymorphism, especially C4, with multiple loci and mutant forms.

    Purpose of the Study:

    • To elucidate the genetic organization and functional implications of complement component genes within the MHC.
    • To investigate the relationship between complement gene polymorphism and susceptibility to autoimmune diseases.

    Main Methods:

    • Gene mapping within the MHC region of humans and mice.
    • Analysis of complement component gene polymorphism, including C4.

    Related Experiment Videos

  • Assessment of haemolytic activity variations among different C4 alleles.

    • Main Results:

    • Established the relative positions of C2, factor B, and C4 genes within the MHC.
    • Identified extensive polymorphism in C4 genes, including variable locus numbers and numerous mutant alleles.
    • Observed significant differences in haemolytic activity among various C4 alleles.

    Conclusions:

    • Complement gene organization within the MHC is conserved between humans and mice.
    • C4 allele-specific differences in haemolytic activity may contribute to the observed associations between HLA haplotypes and autoimmune disease susceptibility.
    • Further research into complement genetics is crucial for understanding autoimmune disease pathogenesis.