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.
Parasite Cell Biology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, 4006, Australia; School of Veterinary Sciences, The University of Queensland, Gatton, 4343, Australia.
Trends Parasitol. 2014 Mar;30(3):141-50. doi: 10.1016/j.pt.2013.12.009. Epub 2014 Jan 13.
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.
在肝血吸虫病中,当血吸虫卵在宿主肝脏中滞留时,会引发白细胞介素 4(IL-4)和 IL-13 介导的优势 CD4+Th2 免疫反应,从而导致肉芽肿和纤维化的形成。在这些过程中,嗜酸性粒细胞、中性粒细胞、巨噬细胞、肝星状细胞和淋巴细胞均被确定为主要的细胞贡献者。本综述概述了肝血吸虫病的细胞和分子机制,重点介绍了主要的细胞成分及其趋化因子的释放。还讨论了曼氏血吸虫和日本血吸虫诱导的肝肉芽肿之间的差异。对与肝血吸虫病相关的过程进行全面概述,可能为改善血吸虫病和其他肉芽肿性疾病的治疗提供新的见解。