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Acquisition of human plasminogen facilitates complement evasion by the malaria parasite Plasmodium falciparum.

Timo ReissHannah I TheisAndres Gonzalez-DelgadoJoel Vega-RodriguezPeter F ZipfelChristine SkerkaGabriele Pradel
Published in: European journal of immunology (2020)
We show that the intraerythrocytic stages of the malaria parasite Plasmodium falciparum bind plasminogen and mediate its conversion into plasmin to inactivate parasite-bound C3b. This complement evasion mechanism counteracts terminal complex formation and hence promotes parasite survival in human blood.
Keyphrases
  • plasmodium falciparum
  • endothelial cells
  • induced pluripotent stem cells
  • pluripotent stem cells
  • free survival
  • toxoplasma gondii