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Plasma immunoglobulin M (IgM) levels dictate complement activation by heparin-platelet factor 4 (PF4) complexes. This natural IgM binding triggers the classical complement pathway, influencing immune responses to heparin and potentially indicating risk for adverse reactions.

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Area of Science:

  • Immunology
  • Complement System Biology

Background:

  • Heparin exposure can trigger antibody responses, but the initiating mechanisms are unclear.
  • Platelet factor 4 (PF4)/heparin complexes activate complement and bind B cells, but the precise initiation is unknown.

Purpose of the Study:

  • To elucidate the initiation mechanisms of complement activation by PF4/heparin complexes.
  • To investigate the role of immunoglobulin M (IgM) in PF4/heparin-mediated complement activation and B cell binding.

Main Methods:

  • Assessed complement activation in healthy donor plasma with varying PF4/heparin concentrations.
  • Utilized proteomic analysis to correlate plasma components with complement activation.
  • Performed IgM depletion and addition experiments to determine IgM's role.
  • Investigated complement activation using cord blood and monoclonal IgM.

Main Results:

  • Plasma complement activation by PF4/heparin showed significant inter-individual variation (high, intermediate, low phenotypes).
  • Complement activation strongly correlated with plasma IgM levels, but not other immunoglobulin isotypes.
  • IgM depletion abrogated C3c generation; adding pooled IgM enhanced activation in low responders.
  • Polyreactive IgM, including natural IgM, activated complement via the classical pathway (C1q dependent) and promoted antigen/complement deposition on B cells.

Conclusions:

  • Variability in plasma IgM levels is linked to functional complement responses to PF4/heparin.
  • Polyreactive IgM binds PF4/heparin, initiating classical complement pathway activation.
  • This process promotes antigen and complement deposition on B cells, offering insights into heparin-induced thrombocytopenia and potential risk biomarkers.