Artikel
Mechanism of complement evasion by malaria parasites
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Autoren
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Thiago F. A. Rosa
- Cellular and Applied Infectionbiology Section, RWTH Aachen University, Aachen, Germany
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Che J. Ngwa
- Cellular and Applied Infectionbiology Section, RWTH Aachen University, Aachen, Germany
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Nina Simon
- Research Center for Infectious Diseases, University of Würzburg, Würzburg, Germany
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Andrea Kuehn
- Research Center for Infectious Diseases, University of Würzburg, Würzburg, Germany
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Edwin Lasonder
- Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
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Vaibhav Agarwal
- Lund University, Malmö, Sweden
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Anna Blom
- Lund University, Malmö, Sweden
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Peter F. Zipfel
- Hans Knöll Institute, Jena, Germany
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Christine Skerka
- Hans Knöll Institute, Jena, Germany
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Gabriele Pradel
- Cellular and Applied Infectionbiology Section, RWTH Aachen University, Aachen, Germany
| Veröffentlicht: | 17. Dezember 2014 |
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Gliederung
Text
The complement system represents a crucial component of the innate immune response against invading pathogens. However, a variety of pathogens evade the complement attack by binding to host complement regulators such factor H, C4b-binding protein or vitronectin. In a recently study we showed that in the mosquito vector, the malaria parasite Plasmodium falciparum binds factor H from the blood meal to inactivate complement factor C3b, thereby protecting the emerging gametes from complement-induced lysis by the blood meal. In consequence, factor H promotes parasites transmission from human to human by the mosquito. While these data provide vital information on a highly complex complement evasion mechanism used by malaria parasites to avoid complement attack in mosquito midgut, it is hitherto not known, if the blood stage parasites in the human host also bind complement regulators for protection. Here, we show that intraerythrocythic schizonts acquire factor H and factor H-like protein 1 from human serum as a mean to evade complement attack in the human host. In contrast, no prominent C4BP binding by schizonts or gametes was detected. The combined data indicate that acquisition of factor H is an important mechanism of the Plasmodium falciparum parasites to protect themselves from attack by the alternative pathway of human complement.
