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Processing of C3b-opsonized immune complexes bound to non-complement receptor 1 (CR1) sites on red cells:

Maria L Craig1, John N Waitumbi, Ronald P Taylor

  • 1Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA 22908, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|February 25, 2005
PubMed

Insights

Immune complexes bound to red blood cells (E) are transferred to macrophages, leading to the loss of complement receptor 1 (CR1) and decay-accelerating factor (DAF). This occurs via antibody-mediated transfer, impacting red blood cell clearance in malaria.

Area of Science:

  • Immunology
  • Hematology
  • Malariology

Background:

  • Severe Plasmodium falciparum malaria in children can cause lethal anemia.
  • Elevated E-bound Abs, reduced E-associated CR1 and DAF, and splenic enlargement suggest a mechanism for E loss involving Abs, complement, and phagocytosis.

Purpose of the Study:

  • To develop an in vitro model to investigate the mechanism of E loss in severe malaria.
  • To examine the transfer of immune complexes (IC) from E to macrophages and the associated loss of complement regulatory proteins.

Main Methods:

  • Incubation of human E with bound Abs and complement (to CR1, DAF, or glycophorin A) with human macrophages (THP-1 cell line).
  • Analysis of IC transfer, E phagocytosis, and the organization/loss of CR1 and DAF.
  • Utilized IgM mAb-C3b and IC-C3b substrates attached to glycophorin A.

Main Results:

  • IC bound to E CR1, DAF, or glycophorin A were transferred to macrophages.
  • DAF was lost from E during DAF-bound IC transfer; CR1-bound IC transfer did not significantly affect DAF levels.
  • CR1, but not DAF, colocalized with IgM mAb-C3b and IC-C3b on glycophorin A, and IgM mAb-C3b binding induced CR1 unclustering.

Conclusions:

  • Antibody-mediated transfer of IC from E to macrophages is a significant mechanism for E loss.
  • This process involves the differential loss of complement regulatory proteins (DAF and CR1) from E.
  • Findings provide insights into the pathogenesis of severe anemia in malaria and potential therapeutic targets.

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