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Although type I IFNs are key drivers of autoantibody production in systemic lupus erythematosus (SLE), their role in bacterial biofilm-induced autoimmunity remains unclear. To address this, we utilized type I IFN receptor-deficient (\n                      <jats:italic toggle=\"yes\">\n                        Ifnar\n                        <jats:sup>\u2212\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      ) mice. Repeated curli administration induced anti-dsDNA autoantibodies independently of IFNAR signaling. We next orally infected C57BL\/6 and\n                      <jats:italic toggle=\"yes\">\n                        Ifnar\n                        <jats:sup>\u2212\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice with a\n                      <jats:italic toggle=\"yes\">Salmonella enterica<\/jats:italic>\n                      serovar Typhimurium (STm) \u0394\n                      <jats:italic toggle=\"yes\">spiB<\/jats:italic>\n                      mutant, which permits long-term colonization without lethal disease. While IFNAR deficiency altered local immune responses and reduced bacterial persistence beginning at 7 days post-infection, it did not affect autoantibody generation. Because extrafollicular splenic responses contribute to both\n                      <jats:italic toggle=\"yes\">Salmonella<\/jats:italic>\n                      immunity and antibody-mediated autoimmunity, we examined germinal center activity and splenic involvement. \u0394\n                      <jats:italic toggle=\"yes\">spiB<\/jats:italic>\n                      infection neither suppressed nor stimulated splenic germinal center formation. Nevertheless, both wild-type and \u0394\n                      <jats:italic toggle=\"yes\">spiB<\/jats:italic>\n                      infections induced anti-dsDNA autoantibodies, suggesting that autoreactive responses occur independently of germinal center activity. Consistent with this, splenectomized mice infected with \u0394\n                      <jats:italic toggle=\"yes\">spiB<\/jats:italic>\n                      produced anti-dsDNA autoantibodies at levels comparable to sham-surgery controls. Together, these findings demonstrate that curli- and\n                      <jats:italic toggle=\"yes\">Salmonella<\/jats:italic>\n                      -induced autoimmunity can arise independently of both type I IFN signaling and the spleen. Our results further identify early gastrointestinal colonization by\n                      <jats:italic toggle=\"yes\">S. Typhimurium<\/jats:italic>\n                      as sufficient to trigger systemic autoreactive responses through mechanisms distinct from classical lupus pathways.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>IMPORTANCE<\/jats:title>\n                    <jats:p>\n                      Persistent colonization of the gastrointestinal tract by bacterial pathogens can have long-term consequences for host immunity that extend beyond the site of infection. Here, we show that intestinal colonization by\n                      <jats:italic toggle=\"yes\">Salmonella enterica<\/jats:italic>\n                      serovar Typhimurium is sufficient to trigger systemic anti-DNA autoantibody responses, even in the absence of type I interferon signaling or the spleen. While type I interferon signaling promoted bacterial persistence, it was dispensable for autoreactive antibody production, revealing that bacterial colonization and autoimmunity can be uncoupled. Unexpectedly, splenectomized mice generated anti-DNA autoantibodies at levels comparable to controls, demonstrating that the spleen is not required for infection-induced autoreactivity. These findings identify early host-microbe interactions in the gut as a key driver of systemic immune dysregulation and highlight how bacterial colonization can shape immune responses and disease outcomes far beyond the intestinal environment.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01478-26","type":"journal-article","created":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T13:04:01Z","timestamp":1785848641000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Contribution of local\n                    <i>Salmonella<\/i>\n                    infection to autoreactivity: divergent roles of type I interferons in colonization and autoantibody production"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-7818-1840","authenticated-orcid":false,"given":"Shingo","family":"Bessho","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00kx1jb78","id-type":"ROR","asserted-by":"publisher"}],"name":"Center for Microbiology and Immunology, Lewis Katz School of Medicine, Temple University","place":["Philadelphia, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaitlyn C. 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