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Phosphorylase-cross-reactive antibodies evoked by streptococcal M protein

J B Dale1, H S Courtney, M Kotb

  • 1Veterans Administration Medical Center, Memphis, Tennessee.

Insights

Antibodies against streptococcal M protein (M5) cross-reacted with muscle phosphorylase enzymes. This cross-reactivity suggests shared epitopes between M protein and phosphorylase, potentially impacting autoimmune responses.

Area of Science:

  • Immunology
  • Biochemistry
  • Molecular Biology

Background:

  • Streptococcal M proteins are key virulence factors.
  • Autoimmunity can arise from molecular mimicry between microbial antigens and host proteins.
  • Phosphorylases are enzymes involved in glycogen metabolism.

Purpose of the Study:

  • To investigate immunological cross-reactivity between streptococcal M5 protein and rabbit muscle phosphorylases.
  • To identify shared epitopes between M protein and phosphorylase.
  • To assess the functional impact of this cross-reactivity on enzyme activity.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) to screen for cross-reactivity.
  • ELISA inhibition studies to confirm epitope sharing.
  • Western blot (immunoblot) analysis to identify reacting protein subunits.
  • Functional assays to measure enzyme inhibition by antibodies.

Main Results:

  • Three of ten rabbit anti-M5 antisera showed significant cross-reactivity with phosphorylase a and b.
  • Cross-reactive antibodies were inhibited by M5, phosphorylase b, M6, and M19, indicating shared epitopes across M protein serotypes.
  • Anti-M5 antibodies recognized the subunit of phosphorylase b and partially inhibited phosphorylase a activity (up to 75%).
  • Enzyme activity was restored upon pre-incubation of antibodies with M5 protein.

Conclusions:

  • Shared epitopes exist between type 5 streptococcal M protein and muscle phosphorylases.
  • These findings suggest a potential mechanism for autoimmune reactions in streptococcal infections.
  • The cross-reactivity has functional consequences, including enzyme inhibition.

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