Complement activation in malaria: Friend or foe?

Sergei Biryukov, Jose Stoute

Research output: Contribution to journalReview article

30 Citations (Scopus)

Abstract

Complement is activated during malaria infection, but there is little evidence that it benefits the host. On the contrary, growing evidence points to the central role of complement activation in the pathogenesis of complicated malaria. Recent evidence suggests a critical role for C5a and the membrane attack complex in the pathogenesis of cerebral malaria, and for C5a in the pathogenesis of placental malaria. In addition, erythrocytes of children with severe malarial anemia have increased deposition of C3b and decreased capacity to regulate complement activation, that probably increase their susceptibility to destruction by liver and splenic macrophages. These observations justify further investigation of the role of complement in malaria and the testing of complement inhibitors as adjunctive treatment for severe malaria.

Original languageEnglish (US)
Pages (from-to)293-301
Number of pages9
JournalTrends in Molecular Medicine
Volume20
Issue number5
DOIs
StatePublished - Jan 1 2014

Fingerprint

Complement Activation
Malaria
Complement Inactivating Agents
Cerebral Malaria
Complement Membrane Attack Complex
Anemia
Erythrocytes
Macrophages
Liver
Infection

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology

Cite this

Biryukov, Sergei ; Stoute, Jose. / Complement activation in malaria : Friend or foe?. In: Trends in Molecular Medicine. 2014 ; Vol. 20, No. 5. pp. 293-301.
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Complement activation in malaria : Friend or foe? / Biryukov, Sergei; Stoute, Jose.

In: Trends in Molecular Medicine, Vol. 20, No. 5, 01.01.2014, p. 293-301.

Research output: Contribution to journalReview article

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T2 - Friend or foe?

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AU - Stoute, Jose

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AB - Complement is activated during malaria infection, but there is little evidence that it benefits the host. On the contrary, growing evidence points to the central role of complement activation in the pathogenesis of complicated malaria. Recent evidence suggests a critical role for C5a and the membrane attack complex in the pathogenesis of cerebral malaria, and for C5a in the pathogenesis of placental malaria. In addition, erythrocytes of children with severe malarial anemia have increased deposition of C3b and decreased capacity to regulate complement activation, that probably increase their susceptibility to destruction by liver and splenic macrophages. These observations justify further investigation of the role of complement in malaria and the testing of complement inhibitors as adjunctive treatment for severe malaria.

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