{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T04:44:10Z","timestamp":1790397850992,"version":"4.1.0"},"reference-count":19,"publisher":"Rockefeller University Press","issue":"11","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,10,20]]},"abstract":"<jats:p>The (patho)physiological role of IgE in nonallergic inflammatory diseases is not well understood. Here, we explored the effect of IgE deficiency on the inflammatory response in Fc\u03b3RIIB-deficient mice as well as in mice carrying both a deletion of Fc\u03b3RIIB and the chromosomal translocation of Y-linked autoimmune acceleration (Yaa) that hastens and results in a more aggressive lupuslike disease in these mice. The findings show that deficiency of IgE delays disease development and severity as demonstrated by reduced autoantibody production and amelioration of organ pathologies. This was associated with decreased numbers of plasma cells and reduced levels of IgG2b and IgG3. Unexpectedly, the loss of IgE also caused a striking decrease of immune cell infiltration in secondary lymphoid organs with a marked effect on the presence of dendritic cells, monocytes, neutrophils, and eosinophils in these organs and decreased activation of basophils. The presence of autoreactive IgE in human systemic lupus erythematosus subjects was also associated with increased basophil activation and enhanced disease activity. These findings argue that IgE facilitates the amplification of autoimmune inflammation.<\/jats:p>","DOI":"10.1084\/jem.20140066","type":"journal-article","created":{"date-parts":[[2014,9,29]],"date-time":"2014-09-29T22:30:00Z","timestamp":1412029800000},"page":"2159-2168","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":89,"title":["Immunoglobulin E plays an immunoregulatory role in lupus"],"prefix":"10.1084","volume":"211","author":[{"given":"Barbara","family":"Dema","sequence":"first","affiliation":[{"name":"Molecular Immunology Section, Laboratory of Molecular Immunogenetics 1 , 2"},{"name":"Office of the Clinical Director, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892 1 , 2"},{"name":"Centre de Recherche sur l\u2019Inflammation, INSERM UMR1149, CNRS ERL8252 Universite Paris Diderot, Laboratoire d\u2019Excellence Inflamex, DHU FIRE, 75018 Paris, 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