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Separation of Plasmodium falciparum Late Stage-infected Erythrocytes by Magnetic Means
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Evasion of Classical Complement Pathway Activation on Plasmodium falciparum-Infected Erythrocytes Opsonized by

Mads Delbo Larsen1,2, Maria Del Pilar Quintana1, Sisse Bolm Ditlev1

  • 1Centre for Medical Parasitology, Department of Immunology and Microbiology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Frontiers in Immunology
|January 23, 2019
PubMed

Insights

Malaria parasites display PfEMP1 proteins on infected red blood cells to evade immune responses. This study reveals how the parasite

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) proteins are key virulence factors in malaria pathogenesis.
  • PfEMP1 proteins are targets of acquired immunity, with IgG1 and IgG3 subclasses dominating the antibody response.
  • Despite antibody binding, complement activation by antibody-opsonized infected erythrocytes (IEs) is not a major immune mechanism.

Purpose of the Study:

  • To investigate the molecular mechanisms preventing classical complement pathway activation by PfEMP1 on infected erythrocytes.
  • To assess complement activation by PfEMP1-specific antibodies using both recombinant and native antigens.
  • To understand parasite evasion strategies against antibody-mediated immunity in malaria.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) to detect complement activation.
  • Flow cytometry to analyze complement activation on infected erythrocytes.
  • Use of polyclonal and monoclonal PfEMP1-specific human IgG.
  • Engineering of a monoclonal antibody for enhanced hexamerization.

Main Results:

  • Polyclonal IgG efficiently activated complement with recombinant VAR2CSA-PfEMP1 in ELISA.
  • No complement activation was detected when the same IgG opsonized native VAR2CSA on IEs.
  • Engineered monoclonal antibodies activated complement in ELISA but not on native VAR2CSA expressed on IEs.

Conclusions:

  • The surface display of PfEMP1 on infected erythrocytes is optimized to inhibit classical complement pathway activation.
  • This represents a novel parasite evasion strategy to circumvent acquired immunity against malaria.
  • Understanding this mechanism could inform new malaria control strategies.
Keywords:
PfEMP1antibodiescomplementevasionknobsmalaria

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