Lack of C3 affects Th2 response development and the sequelae of chemotherapy in schistosomiasis

Anne Camille La Flamme, Andrew S MacDonald, Clive R Huxtable, Michael Carroll, Edward J Pearce

Research output: Contribution to journalArticlepeer-review


The role of the third component of complement (C3) during schistosome infection was investigated using mice deficient in C3. While no effect was observed 8 wk after infection on worm development or liver pathology, Ag-specific Th2-associated cytokine production (IL-13, IL-5, IL-6, and IL-10) was significantly reduced, and IFN-gamma production was enhanced in the absence of C3. IgG1 and IgE, but not IgG2a or IgM, Ab responses were also significantly impaired in infected C3(-/-) mice, suggesting that C3 may play a role in IL-4-mediated Th2 response enhancement during schistosome infection. Furthermore, C3-deficient mice could not effectively clear adult worms after praziquantel (PZQ) treatment and suffered increased morbidity due to the overproduction of proinflammatory mediators following drug administration. However, the ischemic liver damage that normally accompanies PZQ administration in infected wild-type mice was substantially reduced in treated C3-deficient mice, probably due to the absence of dead or dying worms in the livers of these animals. Together these results indicate that C3 enhances Th2 responses during schistosome infection, potentiates PZQ-mediated parasite clearance, and reduces chemotherapy-induced proinflammatory mediator production.
Original languageEnglish
Pages (from-to)470-6
Number of pages7
JournalJournal of Immunology
Issue number1
Publication statusPublished - 2003


  • Animals
  • Anthelmintics
  • Antigens, Helminth
  • Cells, Cultured
  • Complement C3
  • Cytokines
  • Immune Tolerance
  • Inflammation Mediators
  • Liver Diseases, Parasitic
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Morbidity
  • Praziquantel
  • Schistosoma mansoni
  • Schistosomiasis mansoni
  • Th1 Cells
  • Th2 Cells

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