{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T20:23:58Z","timestamp":1783455838215,"version":"3.55.0"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2014,1,3]],"date-time":"2014-01-03T00:00:00Z","timestamp":1388707200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institute of Health","doi-asserted-by":"publisher","award":["R01 NS064059"],"award-info":[{"award-number":["R01 NS064059"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Miller Group Charitable Trust Fund"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,1,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Spontaneous autoimmune polyneuropathy (SAP) in B7-2 knock-out non-obese diabetic (NOD) mice is mediated by myelin protein zero (P0)-reactive T helper type 1 (Th1) cells. In this study, we investigated the role of B cells in SAP, focusing on CD19 as a potential therapeutic target. We found that P0-specific plasmablasts and B cells were increased in spleens of SAP mice compared to wild-type NOD mice. Depletion of B cells and plasmablasts with anti-CD19 monoclonal antibody (mAb) led to attenuation of disease severity when administered at 5 months of age. This was accompanied by decreased serum immunoglobulin (Ig)G and IgM levels, depletion of P0-specific plasmablasts and B cells, down-regulation\/internalization of surface CD19 and increased frequency of CD4+ regulatory T cells in spleens. We conclude that B cells are crucial to the pathogenesis of SAP, and that CD19 is a promising B cell target for the development of disease-modifying agents in autoimmune neuropathies.<\/jats:p>","DOI":"10.1111\/cei.12215","type":"journal-article","created":{"date-parts":[[2013,10,12]],"date-time":"2013-10-12T02:28:42Z","timestamp":1381544922000},"page":"181-191","source":"Crossref","is-referenced-by-count":15,"title":["CD19 as a therapeutic target in a spontaneous autoimmune polyneuropathy"],"prefix":"10.1093","volume":"175","author":[{"given":"P M","family":"Abraham","sequence":"first","affiliation":[{"name":"Department of Neurology, The University of Chicago, Chicago, IL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S H","family":"Quan","sequence":"additional","affiliation":[{"name":"Department of Neurology, The University of Chicago, Chicago, IL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"Dukala","sequence":"additional","affiliation":[{"name":"Department of Neurology, The University of Chicago, Chicago, IL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Soliven","sequence":"additional","affiliation":[{"name":"Department of Neurology, The University of Chicago, Chicago, IL, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,1,3]]},"reference":[{"key":"2021111804104742300_cei12215-bib-0001","doi-asserted-by":"crossref","first-page":"677","DOI":"10.1084\/jem.194.5.677","article-title":"Development of spontaneous autoimmune peripheral polyneuropathy in B7-2-deficient NOD mice","volume":"194","author":"Salomon","year":"2001","journal-title":"J Exp 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