{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,1,2]],"date-time":"2024-01-02T10:48:00Z","timestamp":1704192480324},"reference-count":31,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,10,2]],"date-time":"2014-10-02T00:00:00Z","timestamp":1412208000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2014,11]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Pemphigus vulgaris (<jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>) is an autoimmune skin disease, which has been characterized by IgG autoantibodies to desmoglein 3. Here we studied the antibody signatures of <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content> patients compared with healthy subjects and with patients with two other autoimmune diseases with skin manifestations (systemic lupus erythematosus and scleroderma), using an antigen microarray and informatics analysis. We now report a previously unobserved phenomenon\u00a0\u2013\u00a0patients with <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>, compared with the healthy subjects and the two other diseases, show a significant decrease in IgG autoantibodies to a specific set of self\u2010antigens. This novel finding demonstrates that an autoimmune disease may be associated with a loss of specific, healthy IgG autoantibodies and not only with a gain of specific, pathogenic IgG autoantibodies.<\/jats:p>","DOI":"10.1111\/imm.12316","type":"journal-article","created":{"date-parts":[[2014,5,12]],"date-time":"2014-05-12T14:38:39Z","timestamp":1399905519000},"page":"374-380","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Pemphigus vulgaris is characterized by low IgG reactivities to specific self\u2010antigens along with high IgG reactivity to desmoglein 3"],"prefix":"10.1111","volume":"143","author":[{"given":"Ittai","family":"Fattal","sequence":"first","affiliation":[{"name":"Department of Immunology The Weizmann Institute of Science Rehovot Israel"},{"name":"Department of Physics of Complex Systems The Weizmann Institute of Science Rehovot Israel"},{"name":"Department of Nephrology Rabin Medical Centre Petach Tikva Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jacob","family":"Rimer","sequence":"additional","affiliation":[{"name":"Department of Immunology The Weizmann Institute of Science Rehovot Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Noam","family":"Shental","sequence":"additional","affiliation":[{"name":"Department of Computer Science The Open University of Israel Raanana Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yair","family":"Molad","sequence":"additional","affiliation":[{"name":"The Rheumatology Unit Beilinson Hospital Rabin Medical Centre Petach Tikva Israel"},{"name":"Sackler Faculty of Medicine Tel Aviv University Tel Aviv Israel"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Armando","family":"Gabrielli","sequence":"additional","affiliation":[{"name":"Istituto di Dipartimento di Scienze Cliniche e Molecolari\u2010 Clinica Medica Universit\u00e0 Politecnica delle Marche Ancona 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