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Article: Lack of gastritis and of an adaptive immune response in interferon regulatory factor-1-deficient mice infected with Helicobacter pylori

TitleLack of gastritis and of an adaptive immune response in interferon regulatory factor-1-deficient mice infected with Helicobacter pylori
Authors
KeywordsHelicobacter pylori
Th1
Gastritis
IRF-1
Issue Date2001
Citation
European Journal of Immunology, 2001, v. 31, n. 2, p. 396-402 How to Cite?
AbstractTo study the role of T cell responses in Helicobacter pylori gastritis, C57BL/6 wild-type and interferon regulatory factor-1-deficient (IRF-1-/-) mice were infected with the mouse-adapted H. pylori Sydney strain. Mice lacking the transcription factor IRF-1 are defective in Th1 development and are therefore biased to mount a Th2-type response. After 4 months of infection, C57BL/6 mice developed severe gastritis and atrophy and mounted a Th1-type response towards H. pylori. The Th1 response was abrogated in IRF-1-/- mice. This defective Th1 response was associated with the total lack of gastritis and atrophy in IRF-1-/- mice despite severe colonization with H. pylori. In addition, IRF-1-/- mice did also not develop a Th2 reaction, since they failed to generate H. pylori-specific antibodies and to produce IL-4 in response to H. pylori antigens in vitro. Thus, the transcription factor IRF-1 is necessary for the development of gastritis and atrophy in H. pylori-infected wild-type mice, suggesting a role of Th1 cells in the pathogenesis of H. pylori-associated diseases.
Persistent Identifierhttp://hdl.handle.net/10722/292182
ISSN
2023 Impact Factor: 4.5
2023 SCImago Journal Rankings: 1.627
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSommer, Frank-
dc.contributor.authorFaller, Gerhard-
dc.contributor.authorRöllinghoff, Martin-
dc.contributor.authorKirchner, Thomas-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorLohoff, Michael-
dc.date.accessioned2020-11-17T14:55:56Z-
dc.date.available2020-11-17T14:55:56Z-
dc.date.issued2001-
dc.identifier.citationEuropean Journal of Immunology, 2001, v. 31, n. 2, p. 396-402-
dc.identifier.issn0014-2980-
dc.identifier.urihttp://hdl.handle.net/10722/292182-
dc.description.abstractTo study the role of T cell responses in Helicobacter pylori gastritis, C57BL/6 wild-type and interferon regulatory factor-1-deficient (IRF-1-/-) mice were infected with the mouse-adapted H. pylori Sydney strain. Mice lacking the transcription factor IRF-1 are defective in Th1 development and are therefore biased to mount a Th2-type response. After 4 months of infection, C57BL/6 mice developed severe gastritis and atrophy and mounted a Th1-type response towards H. pylori. The Th1 response was abrogated in IRF-1-/- mice. This defective Th1 response was associated with the total lack of gastritis and atrophy in IRF-1-/- mice despite severe colonization with H. pylori. In addition, IRF-1-/- mice did also not develop a Th2 reaction, since they failed to generate H. pylori-specific antibodies and to produce IL-4 in response to H. pylori antigens in vitro. Thus, the transcription factor IRF-1 is necessary for the development of gastritis and atrophy in H. pylori-infected wild-type mice, suggesting a role of Th1 cells in the pathogenesis of H. pylori-associated diseases.-
dc.languageeng-
dc.relation.ispartofEuropean Journal of Immunology-
dc.subjectHelicobacter pylori-
dc.subjectTh1-
dc.subjectGastritis-
dc.subjectIRF-1-
dc.titleLack of gastritis and of an adaptive immune response in interferon regulatory factor-1-deficient mice infected with Helicobacter pylori-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/1521-4141(200102)31:2<396::AID-IMMU396>3.0.CO;2-Y-
dc.identifier.pmid11180103-
dc.identifier.scopuseid_2-s2.0-0035101139-
dc.identifier.volume31-
dc.identifier.issue2-
dc.identifier.spage396-
dc.identifier.epage402-
dc.identifier.isiWOS:000167029100009-
dc.identifier.issnl0014-2980-

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