{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T16:22:10Z","timestamp":1778602930151,"version":"3.51.4"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2006,11,1]],"date-time":"2006-11-01T00:00:00Z","timestamp":1162339200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Defects within the innate immune system sensitize NF-\u03baB-deficient (p50\u2212\/\u2212; p65+\/\u2212) mice to Helicobacter hepaticus (Hh)-induced colitis. Because IL-10 plays a central role in the inhibition of Hh-induced colitis, we hypothesized that the ability of IL-10 to inhibit the innate inflammatory response to Hh may be compromised in NF-\u03baB-deficient mice. To test this hypothesis, we evaluated the ability of an IL-10-Ig fusion protein with IL-10-like properties to inhibit Hh-induced colitis in RAG-2\u2212\/\u2212 (RAG) and p50\u2212\/\u2212; p65+\/\u2212; RAG-2\u2212\/\u2212 (3X\/RAG) mice. As expected, IL-10-Ig efficiently inhibited the development of colitis in RAG mice. In contrast, the ability of IL-10-Ig to inhibit colitis was compromised in 3X\/RAG mice. The defect in response to IL-10-Ig appeared to be primarily the result of the absence of the p50\/p105 subunit, because the ability of IL-10-Ig to inhibit colitis was also compromised in p50\u2212\/\u2212; RAG-2\u2212\/\u2212 (p50\/RAG) mice. Radiation chimeras demonstrated that the presence of p50\/p105 within hemopoietic cells of the innate immune system was necessary for efficient inhibition of colitis by IL-10-Ig. Consistent with a defect in the suppressive effects of IL-10 in the absence of p50\/p105, we found that the ability of IL-10 to control LPS-induced expression of IL-12 p40 was significantly compromised in macrophages lacking p50\/p105. These results suggest that the absence of the p50\/p105 subunit of NF-\u03baB within hemopoietic cells of the innate immune system interferes with the ability of IL-10 to suppress inflammatory gene expression and Hh-induced colitis.<\/jats:p>","DOI":"10.4049\/jimmunol.177.10.7332","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:39:04Z","timestamp":1397849944000},"page":"7332-7339","source":"Crossref","is-referenced-by-count":31,"title":["Inhibition of\n                    <i>Helicobacter hepaticus<\/i>\n                    -Induced Colitis by IL-10 Requires the p50\/p105 Subunit of NF-\u03baB"],"prefix":"10.1093","volume":"177","author":[{"given":"Michal F","family":"Tomczak","sequence":"first","affiliation":[{"name":"Immunology Research Division, Department of Pathology, Brigham and Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susan E","family":"Erdman","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology , Cambridge, MA 02139"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne","family":"Davidson","sequence":"additional","affiliation":[{"name":"Department of Medicine and Microbiology, Columbia University Medical Center , New York, NY 10032"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan Yan","family":"Wang","sequence":"additional","affiliation":[{"name":"Immunology Research Division, Department of Pathology, Brigham and Women\u2019s Hospital , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Prashant R","family":"Nambiar","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology , Cambridge, MA 02139"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Arlin B","family":"Rogers","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology , Cambridge, MA 02139"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barry","family":"Rickman","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology , Cambridge, MA 02139"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Luchetti","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology , Cambridge, MA 02139"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James G","family":"Fox","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Massachusetts Institute of Technology , Cambridge, MA 02139"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruce H","family":"Horwitz","sequence":"additional","affiliation":[{"name":"Immunology Research Division, Department of Pathology, Brigham and Women\u2019s Hospital , Boston, MA 02115"},{"name":"Division of Emergency Medicine, Children\u2019s Hospital , Boston, MA 02115"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2006,11,15]]},"reference":[{"key":"2026020214063540500_R1","first-page":"521","volume-title":"Nat. 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