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Protection against ...
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Akhiani, Aliasghar,1957Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology
(författare)
Protection against Helicobacter pylori infection following immunization is IL-12-dependent and mediated by Th1 cells
- Artikel/kapitelEngelska2002
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LIBRIS-ID:oai:gup.ub.gu.se/78091
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https://gup.ub.gu.se/publication/78091URI
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The regulatory roles of Th1 and Th2 cells in immune protection against Helicobacter infection are not clearly understood. In this study, we report that a primary H. pylori infection can be established in the absence of IL-12 or IFN-gamma. However, IFN-gamma, but not IL-12, was involved in the development of gastritis because IFN-gamma(-/-) (GKO) mice exhibited significantly less inflammation as compared with IL-12(-/-) or wild-type (WT) mice. Both IL-12(-/-) and GKO mice failed to develop protection following oral immunization with H. pylori lysate and cholera toxin adjuvant. By contrast, Th2-deficient, IL-4(-/-), and WT mice were equally well protected. Mucosal immunization in the presence of coadministered rIL-12 in WT mice increased Ag-specific IFN-gamma-producing T cells by 5-fold and gave an additional 4-fold reduction in colonizing bacteria, confirming a key role of Th1 cells in protection. Importantly, only protected IL-4(-/-) and WT mice demonstrated substantial influx of CD4(+) T cells in the gastric mucosa. The extent of inflammation in challenged IL-12(-/-) and GKO mice was much reduced compared with that in WT mice, indicating that IFN-gamma/Th1 cells also play a major role in postimmunization gastritis. Of note, postimmunization gastritis in IL-4(-/-) mice was significantly milder than WT mice, despite a similar level of protection, indicating that immune protection is not directly linked to the degree of gastric inflammation. Only protected mice had T cells that produced high levels of IFN-gamma to recall Ag, whereas both protected and unprotected mice produced high levels of IL-13. We conclude that IL-12 and Th1 responses are crucial for H. pylori-specific protective immunity.
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Pappo, J.
(författare)
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Kabok, Z.
(författare)
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Schon, K.
(författare)
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Gao, W.
(författare)
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Franzen, L. E.
(författare)
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Lycke, Nils Y,1954Gothenburg University,Göteborgs universitet,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Medical Microbiology/Immunology(Swepub:gu)xlycni
(författare)
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Göteborgs universitetInstitutionen för medicinsk mikrobiologi och immunologi
(creator_code:org_t)
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Ingår i:J Immunol169:12, s. 6977-84
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