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[Fc-receptor proteins of Streptococcus pyogenes and pathogenesis of post-infection complications]

A A Totolian, L A Burova

    Zhurnal Mikrobiologii, Epidemiologii I Immunobiologii
    |October 8, 2014
    PubMed

    Insights

    Group A Streptococcus M proteins bind immunoglobulins, initiating inflammation and organ damage like glomerulonephritis and myocarditis. However, Fc-fragments of immunoglobulin G show potential in suppressing this pathological process.

    Area of Science:

    • Microbiology
    • Immunology
    • Pathology

    Context:

    • Group A Streptococcus (GAS) possesses M proteins that bind immunoglobulins (IgG and IgA) through non-immune mechanisms.
    • These M proteins are key virulence factors contributing to GAS pathogenicity and host tissue damage.
    • The binding of immunoglobulins by M proteins is implicated in the pathogenesis of post-streptococcal sequelae, including kidney and heart inflammation.

    Purpose:

    • To examine the phenomenon and mechanism of non-immune immunoglobulin binding by various GAS emm-genotypes and M-family proteins.
    • To elucidate the role of these receptor proteins in the pathogenesis of post-streptococcal kidney (glomerulonephritis) and heart (myocarditis) damage.
    • To investigate the initiating function of Fc-receptor M proteins in immune inflammation preceding organ damage and to explore novel therapeutic approaches.

    Summary:

    • M proteins of Group A Streptococcus non-immuno-bind immunoglobulins G and A, acting as primary virulence factors.
    • Fc-receptor M proteins initiate immune inflammation in organ tissues by triggering anti-IgG production, immune complex formation, and complement activation, leading to glomerulonephritis and myocarditis.
    • Other GAS factors like cross-reacting antigens and toxins contribute to post-streptococcal processes, mediated by Fc-binding initiated inflammation. Fc-fragments of IgG can suppress this pathology.

    Impact:

    • Provides a deeper understanding of the molecular mechanisms underlying post-streptococcal autoimmune diseases.
    • Identifies Fc-binding M proteins as critical initiators of immune-mediated inflammation in target organs.
    • Suggests a novel therapeutic strategy utilizing Fc-fragments of immunoglobulin G to mitigate streptococcal-induced organ damage.

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