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Since then,\n                    <jats:italic>H. pylori<\/jats:italic>\n                    has been characterized as the primary pathogenic factor for chronic gastritis, peptic ulcer, and gastric malignancy. Numerous patients have received\n                    <jats:italic>H. pylori<\/jats:italic>\n                    eradication treatment, but only 1\u20132% of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    -infected individuals ultimately develop gastric cancer. Recently, numerous epidemiological and basic experimental studies suggested a role for chronic\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection in protecting against inflammatory bowel disease (IBD) by inducing systematic immune tolerance and suppressing inflammatory responses. Here we summarize the current research progress on the association between\n                    <jats:italic>H. pylori<\/jats:italic>\n                    and IBD, and further describe the detailed molecular mechanism underlying\n                    <jats:italic>H. pylori<\/jats:italic>\n                    -induced dendritic cells (DCs) with the tolerogenic phenotype and immunosuppressive regulatory T cells (Tregs). Based on the potential protective role of\n                    <jats:italic>H. pylori<\/jats:italic>\n                    infection on IBD, we suggest that the interaction between\n                    <jats:italic>H. pylori<\/jats:italic>\n                    and the host is complicated, and\n                    <jats:italic>H. pylori<\/jats:italic>\n                    eradication treatment should be administered with caution, especially for children and young adults.\n                  <\/jats:p>","DOI":"10.1038\/s41419-018-0982-2","type":"journal-article","created":{"date-parts":[[2018,9,20]],"date-time":"2018-09-20T10:00:27Z","timestamp":1537437627000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":89,"title":["Helicobacter pylori infection and inflammatory bowel disease: a crosstalk between upper and lower digestive tract"],"prefix":"10.1038","volume":"9","author":[{"given":"Yang","family":"Yu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shengtao","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9595-5536","authenticated-orcid":false,"given":"Li","family":"Min","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2356-4397","authenticated-orcid":false,"given":"Shutian","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2018,9,20]]},"reference":[{"key":"982_CR1","doi-asserted-by":"publisher","first-page":"1590","DOI":"10.1016\/S0140-6736(12)60026-9","volume":"380","author":"DC Baumgart","year":"2012","unstructured":"Baumgart, D. 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