{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:03:03Z","timestamp":1790172183000,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2002,12,1]],"date-time":"2002-12-01T00:00:00Z","timestamp":1038700800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2002,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>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-\u03b3. However, IFN-\u03b3, but not IL-12, was involved in the development of gastritis because IFN-\u03b3\u2212\/\u2212 (GKO) mice exhibited significantly less inflammation as compared with IL-12\u2212\/\u2212 or wild-type (WT) mice. Both IL-12\u2212\/\u2212 and GKO mice failed to develop protection following oral immunization with H. pylori lysate and cholera toxin adjuvant. By contrast, Th2-deficient, IL-4\u2212\/\u2212, and WT mice were equally well protected. Mucosal immunization in the presence of coadministered rIL-12 in WT mice increased Ag-specific IFN-\u03b3-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\u2212\/\u2212 and WT mice demonstrated substantial influx of CD4+ T cells in the gastric mucosa. The extent of inflammation in challenged IL-12\u2212\/\u2212 and GKO mice was much reduced compared with that in WT mice, indicating that IFN-\u03b3\/Th1 cells also play a major role in postimmunization gastritis. Of note, postimmunization gastritis in IL-4\u2212\/\u2212 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-\u03b3 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.<\/jats:p>","DOI":"10.4049\/jimmunol.169.12.6977","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T00:33:07Z","timestamp":1398040387000},"page":"6977-6984","source":"Crossref","is-referenced-by-count":186,"title":["Protection Against <i>Helicobacter pylori<\/i> Infection Following Immunization Is IL-12-Dependent and Mediated by Th1 Cells"],"prefix":"10.1093","volume":"169","author":[{"given":"Ali A","family":"Akhiani","sequence":"first","affiliation":[{"name":"Department of Clinical Immunology, University of Go\u0308teborg , Go\u0308teborg ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacques","family":"Pappo","sequence":"additional","affiliation":[{"name":"Department of Immunology, AstraZeneca R&D Boston , Waltham, MA 02451"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zita","family":"Kabok","sequence":"additional","affiliation":[{"name":"Department of Immunology, AstraZeneca R&D Boston , Waltham, MA 02451"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Scho\u0308n","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, University of Go\u0308teborg , Go\u0308teborg ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Immunology, AstraZeneca R&D Boston , Waltham, MA 02451"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lennart E","family":"Franze\u0301n","sequence":"additional","affiliation":[{"name":"Department of Pathology, O\u0308rebro University Hospital , O\u0308rebro ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nils","family":"Lycke","sequence":"additional","affiliation":[{"name":"Department of Clinical Immunology, University of Go\u0308teborg , Go\u0308teborg ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,12,15]]},"reference":[{"key":"2025032711492492900_R1","first-page":"626","volume-title":"J. 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