Immunopathogenic mechanisms in schistosomiasis: what can be learnt from human studies?

被引:81
作者
Abath, FGC
Morais, CNL
Montenegro, CEL
Wynn, TA
Montenegro, SML
机构
[1] Fdn Oswaldo Cruz, Dept Imunol, Ctr Pesquisas Aggeu Magalhaes, BR-50670420 Recife, PE, Brazil
[2] Univ Fed Pernambuco, Fac Med, BR-50100130 Recife, PE, Brazil
[3] NIAID, Immunopathogenesis Sect Lab Parasit Dis, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.1016/j.pt.2005.12.004
中图分类号
R38 [医学寄生虫学]; Q [生物科学];
学科分类号
07 ; 0710 ; 09 ; 100103 ;
摘要
Studies in mice indicate that schistosome egg-induced granuloma formation and hepatic fibrosis depend markedly on cytokine regulation, with interleukin 10 having a central role. There is no clear consensus about the pattern of cytokine production and regulation that causes a minority of chronically exposed patients to develop severe hepatosplenic (HS) disease, which is characterized by periportal fibrosis and portal hypertension. HS disease and the progression of hepatic fibrosis are associated with the production of profibrotic type 2 cytokines in the early stages of infection with Schistosoma mansoni. However, other studies indicate that HIS disease is characterized by a predominant T helper 1 profile. Until new tools and approaches are developed to study human disease in endemic areas, investigators must either speculate about indirect evidence from human studies or rely more heavily on findings generated from experimental models of the disease.
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页码:85 / 91
页数:7
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