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Cutting Edge: Susceptibility to the Larval Stage of the Helminth ParasiteTaenia crassicepsIs Mediated by Th2 Response Induced Via STAT6 Signaling
Author(s) -
Miriam RodríguezSosa,
John R. David,
Rafael Bojalil,
Abhay R. Satoskar,
Luis I. Terrazas
Publication year - 2002
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.168.7.3135
Subject(s) - taenia crassiceps , biology , parasite hosting , stat6 , immunology , immune system , immunity , microbiology and biotechnology , interleukin 13 , helminths , nitric oxide , ascaris suum , interleukin 4 , endocrinology , cestoda , world wide web , computer science
Using STAT6(-/-) BALB/c mice, we analyzed the role of STAT6-induced Th2 response in determining the outcome of murine cysticercosis caused by the helminth parasite Taenia crassiceps. After T. crassiceps infection, wild-type BALB/c mice developed a strong Th2-like response; produced high levels of IgG1, IgE, IL-4, as well as IL-13; and remained susceptible to T. crassiceps. In contrast, similarly infected STAT6(-/-) mice mounted a strong Th1-like response; produced high levels of IgG2a, IL-12, IFN-gamma, as well as nitric oxide; and efficiently controlled T. crassiceps infection. These findings demonstrate that Th2-like response induced via STAT6-mediated signaling pathway mediates susceptibility to T. crassiceps and, furthermore, that unlike the case in most helminths, immunity against T. crassiceps is mediated by a Th1-like rather than Th2-like response.

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