{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T11:02:04Z","timestamp":1768906924090,"version":"3.49.0"},"reference-count":43,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2006,2,10]],"date-time":"2006-02-10T00:00:00Z","timestamp":1139529600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL58688"],"award-info":[{"award-number":["HL58688"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["HL67040"],"award-info":[{"award-number":["HL67040"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005615","name":"Beth Israel Deaconess Medical Center","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100005615","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    This investigation focused on obtaining a further understanding of the role of heme oxygenase\u20101 (HO\u20101) in tolerance induction. Hearts from C57BL\/6 (H\u20102\n                    <jats:sup>b<\/jats:sup>\n                    ) mice survived long\u2010term when transplanted into BALB\/c (H\u20102\n                    <jats:sup>d<\/jats:sup>\n                    ) recipients treated with the tolerance\u2010inducing regimen of anti\u2010CD40L antibody (MR\u20101) plus donor\u2010specific transfusion (DST). Grafts did not, however, survive long\u2010term in (HO\u20101\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) recipients given the same treatment. Similarly, long\u2010term survival induced by DST was ablated when HO\u20101 activity was blocked by zinc protoporphyrin IX (ZnPPIX). We further asked whether modulation of HO\u20101 expression\/activity could be used to promote the induction of graft tolerance. DST alone (day 0) failed to promote any prolongation of survival of DBA\/2 (H\u20102\n                    <jats:sup>d<\/jats:sup>\n                    ) hearts transplanted into B6AF1 (H\u20102\n                    <jats:sup>b,k\/d<\/jats:sup>\n                    ) recipients. However, long\u2010term survival and (dominant peripheral) tolerance were readily induced when DST was combined with induction of HO\u20101 expression by cobalt protoporphyrin IX (CoPPIX). HO\u20101 induction plus DST led to a significant up\u2010regulation of\n                    <jats:italic>Foxp3<\/jats:italic>\n                    , TGF\u2010\u03b2, IL\u201010, and CTLA4, which suggests a prominent role for CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>+<\/jats:sup>\n                    regulatory T cells (Tregs). In fact, the tolerogenic effect of HO\u20101 plus DST was dependent on CD4\n                    <jats:sup>+<\/jats:sup>\n                    CD25\n                    <jats:sup>+<\/jats:sup>\n                    Tregs as suggested by adoptively transferring these cells into irradiated recipients under various regimens. Taken together, these findings show that expression of HO\u20101 in a graft recipient can be essential for long\u2010term graft survival and for induction of tolerance and that modulation of HO\u20101 expression\/activity can be used therapeutically to synergize in the generation of graft tolerance.\n                  <\/jats:p>","DOI":"10.1096\/fj.05-4791fje","type":"journal-article","created":{"date-parts":[[2006,2,10]],"date-time":"2006-02-10T20:24:11Z","timestamp":1139603051000},"page":"776-778","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":84,"title":["Heme oxygenase\u20101 is essential for and promotes tolerance to transplanted organs"],"prefix":"10.1096","volume":"20","author":[{"given":"Kenichiro","family":"Yamashita","sequence":"first","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]},{"given":"Robert","family":"\u00d6llinger","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"},{"name":"Department of Surgery Medical University of Innsbruck  Austria"}]},{"given":"James","family":"McDaid","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]},{"given":"Hideyasu","family":"Sakahama","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]},{"given":"Hongjun","family":"Wang","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]},{"given":"Shivraj","family":"Tyagi","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]},{"given":"Eva","family":"Csizmadia","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]},{"given":"Neal R.","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Pathology Massachusetts General Hospital Harvard Medical School Boston Massachusetts"}]},{"given":"Miguel P.","family":"Soares","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"},{"name":"Instituto Gulbenkian de Ci\u00eancia  Apartado 14 2781\u2013901 Oeiras Portugal"}]},{"given":"Fritz H.","family":"Bach","sequence":"additional","affiliation":[{"name":"Immunobiology Research Center Department of Surgery Beth Israel Deaconess Medical Center Harvard Medical School  Boston Massachusetts"}]}],"member":"311","published-online":{"date-parts":[[2006,2,10]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm1251"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1097\/01.TP.0000106469.12073.01"},{"key":"e_1_2_6_4_1","first-page":"1171","article-title":"Clonal deletion as a mechanism of transplantation tolerance","volume":"15","author":"Nikolic B.","year":"1996","journal-title":"J. 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