{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T01:26:54Z","timestamp":1770082014739,"version":"3.49.0"},"reference-count":31,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2001,8,1]],"date-time":"2001-08-01T00:00:00Z","timestamp":996624000000},"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":[[2001,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Transgenic restoration of normally absent H2-E MHC class II molecules on APC dominantly inhibits T cell-mediated autoimmune diabetes (IDDM) in nonobese diabetic (NOD) mice. We analyzed the minimal requirements for transgenic H2-E expression on APC subtypes (B lymphocytes vs macrophages\/dendritic cells (DC)) to inhibit IDDM. This issue was addressed through the use of NOD stocks transgenically expressing high levels of H2-E and\/or made genetically deficient in B lymphocytes in a series of genetic intercross and bone marrow\/lymphocyte chimera experiments. Standard (H2-Enull) NOD B lymphocytes exert a pathogenic function(s) necessary for IDDM. However, IDDM was inhibited in mixed chimeras where H2-E was solely expressed on all B lymphocytes. Interestingly, this resistance was abrogated when even a minority of standard NOD H2-Enull B lymphocytes were also present. In contrast, in NOD chimeras where H2-E expression was solely limited to approximately half the macrophages\/DC, an active immunoregulatory process was induced that inhibited IDDM. Introduction of a disrupted IL-4 gene into the NOD-H2-E transgenic stock demonstrated that induction of this Th2 cytokine does not represent the IDDM protective immunoregulatory process mediated by H2-E expression. In conclusion, high numbers of multiple subtypes of APC must express H2-E MHC class II molecules to additively inhibit IDDM in NOD mice. This raises a high threshold for success in future intervention protocols designed to inhibit IDDM by introduction of putatively protective MHC molecules into hemopoietic precursors of APC.<\/jats:p>","DOI":"10.4049\/jimmunol.167.4.2404","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T19:18:03Z","timestamp":1398194283000},"page":"2404-2410","source":"Crossref","is-referenced-by-count":31,"title":["Inhibition of Autoimmune Diabetes in Nonobese Diabetic Mice by Transgenic Restoration of H2-E MHC Class II Expression: Additive, But Unequal, Involvement of Multiple APC Subtypes"],"prefix":"10.1093","volume":"167","author":[{"given":"Ellis A","family":"Johnson","sequence":"first","affiliation":[{"name":"The Jackson Laboratory , Bar Harbor, ME 04609"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pablo","family":"Silveira","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory , Bar Harbor, ME 04609"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harold D","family":"Chapman","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory , Bar Harbor, ME 04609"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edward H","family":"Leiter","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory , Bar Harbor, ME 04609"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David V","family":"Serreze","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory , Bar Harbor, ME 04609"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2001,8,15]]},"reference":[{"key":"2026020209112101300_R1","first-page":"291","volume-title":"Immunity","year":"1997"},{"key":"2026020209112101300_R2","first-page":"71","volume-title":"NOD Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, and Other Diseases","year":"1998"},{"key":"2026020209112101300_R3","first-page":"179","volume-title":"Annu. 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