{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T13:05:50Z","timestamp":1790859950431,"version":"4.1.0"},"reference-count":100,"publisher":"Oxford University Press (OUP)","issue":"1038","license":[{"start":{"date-parts":[[2012,2,10]],"date-time":"2012-02-10T00:00:00Z","timestamp":1328832000000},"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":[[2012,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>More than 60\u2005years ago, Burnet first proposed the \u2018forbidden clone\u2019 hypothesis postulating that autoimmune disease arises as a result of persistence of self-reactive clones of lymphocytes that should have been deleted via immune tolerance. These autoreactive clones could effect immune-mediated end-organ damage via peripheral self-antigen recognition. Recent evidence that stretches across the boundaries of many medical specialties supports this proposal, implicating a B cell precursor as the culprit. The success of B cell depleting therapy in rheumatoid arthritis, anti-neutrophil cytoplasmic antibodies (ANCA) associated vasculitis, polymyositis, lupus and autoimmune diseases as diverse as multiple sclerosis and idiopathic thrombocytopenic purpura supports this proposal. Clonality of B cells and plasma cells has been described in a number of autoimmune disorders and the presence of autoantibodies, which may arise years before the onset of clinical disease, supports the notion of autoreactivity within the B cell lineage. T cell activation within the end-organ would be predicted by cognate B\u2013T cell interactions and resultant tissue inflammation and destruction could produce diverse clinical manifestations dictated by the original specificity of the autoimmune B cell.<\/jats:p>","DOI":"10.1136\/postgradmedj-2011-130364","type":"journal-article","created":{"date-parts":[[2012,2,11]],"date-time":"2012-02-11T03:43:37Z","timestamp":1328931817000},"page":"226-233","source":"Crossref","is-referenced-by-count":19,"title":["A B cell explanation for autoimmune disease: the forbidden clone returns"],"prefix":"10.1093","volume":"88","author":[{"given":"Fiona","family":"McQueen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,2,10]]},"reference":[{"key":"2023041906373265600_bib1","first-page":"3","article-title":"The Nobel Lectures in Immunology. The Nobel Prize for Physiology or Medicine, 1960. 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