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Using adoptive transfer into<jats:italic>H. pylori<\/jats:italic>-infected Rag2<jats:sup>\u2212\/\u2212<\/jats:sup>mice, we evaluated effects of wild-type (wt) C57BL\/6 or congenic interleukin-10-deficient (IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>) T<jats:sub>R<\/jats:sub>cells on gastritis, gastric cytokines, and<jats:italic>H. pylori<\/jats:italic>colonization. Infected Rag2<jats:sup>\u2212\/\u2212<\/jats:sup>mice colonized in the corpus and antrum with 10<jats:sup>5<\/jats:sup>to 10<jats:sup>6<\/jats:sup><jats:italic>H. pylori<\/jats:italic>CFU\/gram without associated gastritis. T<jats:sub>E<\/jats:sub>cell transfer caused morbidity and an<jats:italic>H. pylori<\/jats:italic>-independent pangastritis and duodenitis (gastroduodenitis) associated with increased expression of gamma interferon (IFN-\u03b3) and tumor necrosis factor alpha. T<jats:sub>E<\/jats:sub>cell transfer to<jats:italic>H. pylori<\/jats:italic>-infected mice led to additive corpus gastritis associated with inflammatory cytokine expression and reduced colonization. wt T<jats:sub>R<\/jats:sub>cells reduced morbidity,<jats:italic>H. pylori<\/jats:italic>corpus gastritis, gastroduodenitis, and inflammatory cytokine expression and reversed the decline in<jats:italic>H. pylori<\/jats:italic>colonization attributable to T<jats:sub>E<\/jats:sub>cells. Although less effective than wt T<jats:sub>R<\/jats:sub>cells, IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>T<jats:sub>R<\/jats:sub>cells also reduced morbidity and gastroduodenitis but did not reduce<jats:italic>H. pylori<\/jats:italic>corpus gastritis or impact T<jats:sub>E<\/jats:sub>cell inhibition of colonization. Gastric tissues from mice receiving wt T<jats:sub>R<\/jats:sub>cells expressed higher levels of Foxp3 compared to recipients of IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>T<jats:sub>R<\/jats:sub>cells, consistent with lower regulatory activity of IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>T<jats:sub>R<\/jats:sub>cells. These results demonstrate that wt T<jats:sub>R<\/jats:sub>cells suppressed T<jats:sub>E<\/jats:sub>-cell-mediated<jats:italic>H. pylori<\/jats:italic>-independent gastroduodenitis and<jats:italic>H. pylori<\/jats:italic>-dependent corpus gastritis more effectively than IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>T<jats:sub>R<\/jats:sub>cells. Compartmental differences in T<jats:sub>E<\/jats:sub>-cell- and<jats:italic>H. pylori<\/jats:italic>-mediated inflammation and in regulatory effects between wt T<jats:sub>R<\/jats:sub>and IL-10<jats:sup>\u2212\/\u2212<\/jats:sup>T<jats:sub>R<\/jats:sub>cells suggest that IL-10 expression by wt T<jats:sub>R<\/jats:sub>cells is important to regulatory suppression of gastric inflammation.<\/jats:p>","DOI":"10.1128\/iai.01788-06","type":"journal-article","created":{"date-parts":[[2007,3,13]],"date-time":"2007-03-13T05:34:26Z","timestamp":1173764066000},"page":"2699-2707","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["Wild-Type and Interleukin-10-Deficient Regulatory T Cells Reduce Effector T-Cell-Mediated Gastroduodenitis in Rag2<sup>\u2212\/\u2212<\/sup>Mice, but Only Wild-Type Regulatory T Cells Suppress<i>Helicobacter pylori<\/i>Gastritis"],"prefix":"10.1128","volume":"75","author":[{"given":"Chung-Wei","family":"Lee","sequence":"first","affiliation":[{"name":"Division of Comparative Medicine"},{"name":"Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Varada P.","family":"Rao","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arlin B.","family":"Rogers","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhongming","family":"Ge","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan E.","family":"Erdman","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark T.","family":"Whary","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James G.","family":"Fox","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine"},{"name":"Biological Engineering Division, Massachusetts Institute of Technology, Cambridge, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.9.5306"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.166.5.3008"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.190.7.995"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200636459"},{"key":"e_1_3_2_6_2","first-page":"1377","volume":"152","year":"1998","unstructured":"Berg, D. 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