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Splenic uptake of immune complexes in man is complement-dependent

K A Davies1, K Erlendsson, H L Beynon

  • 1Department of Medicine, Hammersmith Hospital, London, United Kingdom.

Journal of Immunology (Baltimore, Md. : 1950)
|October 1, 1993
PubMed
Summary

Hereditary C2 deficiency impairs immune complex processing, leading to rapid liver uptake and no spleen uptake. Restoring complement activity with fresh frozen plasma normalizes clearance and enables spleen uptake, suggesting a link to SLE predisposition.

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Area of Science:

  • Immunology
  • Complement System
  • Autoimmunity

Background:

  • Hereditary C2 deficiency affects the classical complement pathway.
  • Immune complex (IC) processing is crucial for immune homeostasis.
  • Defects in complement may predispose individuals to autoimmune diseases like SLE.

Purpose of the Study:

  • To investigate the impact of C2 deficiency on radiolabeled immune complex processing.
  • To evaluate the role of complement in immune complex clearance and tissue localization.
  • To explore the potential link between complement deficiency and SLE pathogenesis.

Main Methods:

  • Studied a patient with homozygous C2 deficiency before and after fresh frozen plasma (FFP) treatment.
  • Utilized radiolabeled Hepatitis B surface antigen/antibody immune complexes (IC).

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  • Employed dynamic and static gamma-scintigraphy for clearance and uptake analysis.

    • Main Results:

    • Before FFP treatment (zero C2/CH50), rapid liver uptake (t90% = 13.6 min) and clearance (t1/2 = 6.8 min) of IC occurred, with no splenic uptake.
    • After FFP normalization of complement, IC clearance slowed (t1/2 = 9.8 min, t90% = 27 min), and splenic uptake increased to 20%.
    • Erythrocyte CR1 binding to IC was minimal in C2 deficiency but increased post-treatment, similar to normal subjects.

    Conclusions:

    • Splenic uptake of immune complexes in humans is dependent on complement activity.
    • Abnormal immune complex processing due to complement deficiency may contribute to the predisposition to Systemic Lupus Erythematosus (SLE).
    • FFP can temporarily restore classical complement pathway function and normalize IC processing.