{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,22]],"date-time":"2026-08-22T22:13:29Z","timestamp":1787436809414,"version":"build-2736575974"},"reference-count":73,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2025,1,6]],"date-time":"2025-01-06T00:00:00Z","timestamp":1736121600000},"content-version":"vor","delay-in-days":280,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Helicobacter pylori is a Gram-negative pathogen that colonizes the stomach, induces inflammation, and drives pathological changes in the stomach tissue, including gastric cancer. As the principal cytokine produced by Th17 cells, IL-17 mediates protective immunity against pathogens by inducing the activation and mobilization of neutrophils. Whereas IL-17A is largely produced by lymphocytes, the IL-17 receptor is expressed in epithelial cells, fibroblasts, and hematopoietic cells. Loss of the IL-17RA in mice results in impaired antimicrobial responses to extracellular bacteria. In the context of H. pylori infection, this is compounded by extensive inflammation in Il17ra\u2212\/\u2212 mice. In this study, Foxa3creIl17rafl\/fl (Il17ra\u0394GI-Epi) and Il17rafl\/fl (control) mice were used to test the hypothesis that IL-17RA signaling, specifically in epithelial cells, protects against severe inflammation after H. pylori infection. The data indicate that Il17ra\u0394GI-Epi mice develop increased inflammation compared with controls. Despite reduced Pigr expression, levels of IgA increased in the gastric wash, suggesting significant increase in Ag-specific activation of the T follicular helper\/B cell axis. Gene expression analysis of stomach tissues indicate that both acute and chronic responses are significantly increased in Il17ra\u0394GI-Epi mice compared with controls. These data suggest that a deficiency of IL-17RA in epithelial cells is sufficient to drive chronic inflammation and hyperactivation of the Th17\/T follicular helper\/B cell axis but is not required for recruitment of polymorphonuclear neutrophils. Furthermore, the data suggest that fibroblasts can produce chemokines in response to IL-17 and may contribute to H. pylori\u2013induced inflammation through this pathway.<\/jats:p>","DOI":"10.4049\/immunohorizons.2300078","type":"journal-article","created":{"date-parts":[[2024,4,19]],"date-time":"2024-04-19T08:25:27Z","timestamp":1713515127000},"page":"339-353","source":"Crossref","is-referenced-by-count":6,"title":["IL-17RA\u2013Mediated Epithelial Cell Activity Prevents Severe Inflammatory Response to\n                    <i>Helicobacter pylori<\/i>\n                    Infection"],"prefix":"10.1093","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-2142-9658","authenticated-orcid":false,"given":"Lee C","family":"Brackman","sequence":"first","affiliation":[{"name":"Tennessee Valley Healthcare System, Department of Veterans Affairs , Nashville, TN"},{"name":"Division of Infectious Disease, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0005-1700-4870","authenticated-orcid":false,"given":"Matthew S","family":"Jung","sequence":"additional","affiliation":[{"name":"Tennessee Valley Healthcare System, Department of Veterans Affairs , Nashville, TN"},{"name":"Division of Infectious Disease, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5754-5798","authenticated-orcid":false,"given":"Eseoghene I","family":"Ogaga","sequence":"additional","affiliation":[{"name":"Tennessee Valley Healthcare System, Department of Veterans Affairs , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nikhita","family":"Joshi","sequence":"additional","affiliation":[{"name":"Tennessee Valley Healthcare System, Department of Veterans Affairs , Nashville, TN"},{"name":"Vanderbilt University, School of Biological Sciences , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lydia E","family":"Wroblewski","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0000-1324","authenticated-orcid":false,"given":"M Blanca","family":"Piazuelo","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4836-5960","authenticated-orcid":false,"suffix":"Jr.","given":"Richard M","family":"Peek","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1717-4472","authenticated-orcid":false,"given":"Yash A","family":"Choksi","sequence":"additional","affiliation":[{"name":"Tennessee Valley Healthcare System, Department of Veterans Affairs , Nashville, TN"},{"name":"Division of Gastroenterology, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3735-4649","authenticated-orcid":false,"given":"Holly M Scott","family":"Algood","sequence":"additional","affiliation":[{"name":"Tennessee Valley Healthcare System, Department of Veterans Affairs , Nashville, TN"},{"name":"Division of Infectious Disease, Department of Medicine, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"},{"name":"Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Vanderbilt University Medical Center , Nashville, TN"},{"name":"Vanderbilt Institute of Infection, Immunity, and Inflammation, Vanderbilt University Medical Center , Nashville, TN"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,4,19]]},"reference":[{"key":"2025010608551384500_r1","doi-asserted-by":"crossref","first-page":"713","DOI":"10.1128\/CMR.00011-10","article-title":"Helicobacter pylori and gastric cancer: factors that modulate disease risk","volume":"23","author":"Wroblewski","year":"2010","journal-title":"Clin. 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