{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T04:58:58Z","timestamp":1790917138480,"version":"4.1.0"},"reference-count":51,"publisher":"Rockefeller University Press","issue":"7","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1997,4,7]]},"abstract":"<jats:p>RelB-deficient mice (relB\u2212\/\u2212) have a complex phenotype including multiorgan inflammation and hematopoietic abnormalities. To examine whether other NF-\u03baB\/Rel family members are required for the development of this phenotype or have a compensatory role, we have initiated a program to generate double-mutant mice that are deficient in more than one family member. Here we report the phenotypic changes in relB\u2212\/\u2212 mice that also lack the p50 subunit of NF\u03baB (p50\u2212\/\u2212). The inflammatory phenotype of p50\u2212\/\u2212relB\u2212\/\u2212 double-mutant mice was markedly increased in both severity and extent of organ involvement, leading to premature death within three to four weeks after birth. Double-knockout mice also had strongly increased myeloid hyperplasia and thymic atrophy. Moreover, B cell development was impaired and, in contrast to relB\u2212\/\u2212 single knockouts, B cells were absent from inflammatory infiltrates. Both p50\u2212\/\u2212 and heterozygous relB\u2212\/+ animals are disease-free. In the absence of the p50, however, relB\u2212\/+ mice (p50\u2212\/\u2212relB\u2212\/+) had a mild inflammatory phenotype and moderate myeloid hyperplasia. Neither elevated mRNA levels of other family members, nor increased \u03baB-binding activities of NF-\u03baB\/Rel complexes could be detected in single- or double-mutant mice compared to control animals. These results indicate that the lack of RelB is, in part, compensated by other p50-containing complexes and that the \u201cclassical\u201d p50-RelA\u2013NF-\u03baB activity is not required for the development of the inflammatory phenotype.<\/jats:p>","DOI":"10.1084\/jem.185.7.1359","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:49:30Z","timestamp":1027702170000},"page":"1359-1370","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":94,"title":["p50\u2013NF-\u03baB Complexes Partially Compensate for the Absence of RelB: Severely Increased Pathology in <i>p50\u2212<\/i>\/\u2212<i>relB\u2212<\/i>\/\u2212Double-knockout Mice"],"prefix":"10.1084","volume":"185","author":[{"given":"Falk","family":"Weih","sequence":"first","affiliation":[{"name":"From the *Department of Oncology, \u2021Department of Experimental Pathology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the \u00a7Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen K.","family":"Durham","sequence":"additional","affiliation":[{"name":"From the *Department of Oncology, \u2021Department of Experimental Pathology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the \u00a7Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Debra S.","family":"Barton","sequence":"additional","affiliation":[{"name":"From the *Department of Oncology, \u2021Department of Experimental Pathology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the \u00a7Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William C.","family":"Sha","sequence":"additional","affiliation":[{"name":"From the *Department of Oncology, \u2021Department of Experimental Pathology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the \u00a7Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Baltimore","sequence":"additional","affiliation":[{"name":"From the *Department of Oncology, \u2021Department of Experimental Pathology, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey 08543-4000; and the \u00a7Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rodrigo","family":"Bravo","sequence":"additional","affiliation":[{"name":"From the *Department of 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