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Related Experiment Videos

Complement activation and spleen function in erythema multiforme associated with herpes simplex virus reactivation.

M H Wansbrough-Jones, D M Collas, S Bishop

    Journal of Clinical & Laboratory Immunology
    |October 1, 1986
    PubMed
    Summary

    This study found that while C3d levels rise during cold sores, they do not increase during erythema multiforme (EM). However, prolonged clearance of damaged red blood cells during EM suggests immune complexes may spread herpes simplex virus antigens before EM onset.

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    Warm autoadsorption with enzyme-treated red blood cells.

    Immunohematology·2013

    Area of Science:

    • Immunology
    • Dermatology
    • Virology

    Background:

    • Erythema multiforme (EM) is a skin condition often linked to infections, particularly herpes simplex virus (HSV).
    • The exact immunological mechanisms triggering EM remain incompletely understood.
    • Immune complexes are implicated in various inflammatory conditions.

    Purpose of the Study:

    • To investigate plasma C3d concentrations and red blood cell clearance in patients with erythema multiforme complicating herpes labialis.
    • To explore the role of immune complexes in the pathogenesis of EM.
    • To determine if C3d levels correlate with EM or its preceding herpes labialis (cold sores).

    Main Methods:

    • Measurement of plasma C3d concentrations in patients during active cold sores and during EM episodes.

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  • Assessment of heat-damaged red blood cell clearance rates in patients with EM.
  • Comparison of C3d levels and red blood cell clearance between different disease states.
  • Main Results:

    • Plasma C3d concentrations were elevated during herpes labialis (cold sores) but not during erythema multiforme (EM).
    • Heat-damaged red blood cell clearance was significantly prolonged in patients experiencing EM.
    • These findings suggest a dissociation between C3d levels and active EM.

    Conclusions:

    • The prolonged clearance of damaged red cells during EM, despite normal C3d levels, supports a role for immune complexes in EM pathogenesis.
    • These observations suggest that herpes simplex virus (HSV) antigens may disseminate via immune complexes to the skin prior to the clinical onset of EM.
    • Further research is warranted to elucidate the precise role of immune complexes in EM development.