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Here, we investigate mechanisms by which Salmonella-superspreader (SSP) hosts maintain an asymptomatic state during chronic infection. We found that regulatory T cells (Tregs) are essential for this disease-tolerant state, limiting intestinal immunopathology and enabling SSP hosts to thrive, while facilitating Salmonella transmission. Treg depletion in SSP mice resulted in decreased survival, heightened gut inflammation, and impairment of the intestinal barrier, without affecting Salmonella persistence. Colonic Tregs from SSP mice exhibited a unique transcriptomic profile characterized by the upregulation of type 1 inflammatory genes, including the transcription factor T-bet. In the absence of Tregs, we observed robust expansion of cytotoxic CD4+ T cells, with CD4+ T cell depletion restoring homeostasis. These results uncover a critical host strategy to establish disease tolerance during chronic enteric infection, providing novel insights into mucosal responses to persistent pathogens and chronic intestinal inflammation.<\/jats:p>","DOI":"10.1084\/jem.20242431","type":"journal-article","created":{"date-parts":[[2025,8,8]],"date-time":"2025-08-08T06:20:42Z","timestamp":1754634042000},"update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["<i>Salmonella<\/i>\n                    -superspreader hosts require gut regulatory T cells to maintain a disease-tolerant state"],"prefix":"10.1084","volume":"222","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0137-953X","authenticated-orcid":true,"given":"Blanda","family":"Di Luccia","sequence":"first","affiliation":[{"name":"Stanford University School of Medicine 1 Department of Microbiology and Immunology, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8938-9507","authenticated-orcid":true,"given":"Liliana M.","family":"Massis","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 1 Department of Microbiology and Immunology, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6717-545X","authenticated-orcid":true,"given":"Daniel S.C.","family":"Butler","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 1 Department of Microbiology and Immunology, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2581-2342","authenticated-orcid":true,"given":"Ramya","family":"Narasimhan","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 1 Department of Microbiology and Immunology, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2799-1222","authenticated-orcid":true,"given":"Sarah J.","family":"Ruddle","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/0046gcs23","id-type":"ROR","asserted-by":"publisher"}],"name":"Max Planck Institute for Infection Biology 2 Department of Cellular Microbiology, , Berlin,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2724-2547","authenticated-orcid":true,"given":"Trung H.M.","family":"Pham","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 1 Department of Microbiology and Immunology, , Stanford, CA,","place":["USA"]},{"name":"Stanford University School of Medicine 3 Department of Pediatrics, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3341-2258","authenticated-orcid":true,"given":"Jos\u00e9 G.","family":"Vilches-Moure","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 4 Department of Comparative Medicine, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3804-2209","authenticated-orcid":true,"given":"Denise M.","family":"Monack","sequence":"additional","affiliation":[{"name":"Stanford University School of Medicine 1 Department of Microbiology and Immunology, , Stanford, CA,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2025,9,9]]},"reference":[{"key":"2025090909482624500_bib1","doi-asserted-by":"publisher","first-page":"197","DOI":"10.1111\/imm.12602","article-title":"Plasmodium yoelii infection of BALB\/c mice results in expansion rather than induction of CD4(+) Foxp3(+) regulatory T cells","volume":"148","author":"Abel","year":"2016","journal-title":"Immunology"},{"key":"2025090909482624500_bib2","doi-asserted-by":"publisher","first-page":"199","DOI":"10.1053\/j.gastro.2010.06.047","article-title":"Tolerance rather than immunity protects from Helicobacter pylori-induced gastric preneoplasia","volume":"140","author":"Arnold","year":"2011","journal-title":"Gastroenterology"},{"key":"2025090909482624500_bib3","doi-asserted-by":"publisher","first-page":"119","DOI":"10.1038\/nri2916","article-title":"Phenotypical and functional specialization of FOXP3+ regulatory T cells","volume":"11","author":"Campbell","year":"2011","journal-title":"Nat. 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