Affiliations 

  • 1 Parasite Cell Biology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Australia; School of Veterinary Sciences, The University of Queensland, Gatton, 4343, Australia; School of Medical Sciences, Universiti Sains Malaysia, 16150, Kelantan, Malaysia
  • 2 Parasite Cell Biology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Australia; School of Veterinary Sciences, The University of Queensland, Gatton, 4343, Australia
  • 3 Division of Mycobacterial Research, National Institute for Medical Research, London, NW7 1AA, UK
  • 4 Molecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Australia
  • 5 Molecular Parasitology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Australia. Electronic address: [email protected]
Trends Parasitol, 2014 Mar;30(3):141-50.
PMID: 24433721 DOI: 10.1016/j.pt.2013.12.009

Abstract

In hepatic schistosomiasis, pathology arises when schistosome eggs become lodged in the host liver, evoking an interleukin 4 (IL-4)- and IL-13-mediated dominant CD4(+) Th2 immune response. This response leads to the development of granulomas and fibrosis, with eosinophils, neutrophils, macrophages, hepatic stellate cells, and lymphocytes all identified as major cellular contributors to these events. This review outlines the cellular and molecular mechanisms of hepatic schistosomiasis, with an emphasis on the major cellular components and their release of chemokines. The differences between Schistosoma mansoni- and Schistosoma japonicum-induced hepatic granuloma are also discussed. This comprehensive overview of the processes associated with hepatic schistosomiasis may provide new insights into improved treatment for both schistosomiasis and other granulofibrotic diseases.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.