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- W2026152073 abstract "To 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." @default.
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- W2026152073 date "2001-02-01" @default.
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- W2026152073 title "Lack of gastritis and of an adaptive immune response in interferon regulatory factor-1-deficient mice infected withHelicobacter pylori" @default.
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- W2026152073 doi "https://doi.org/10.1002/1521-4141(200102)31:2<396::aid-immu396>3.0.co;2-y" @default.
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