{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T10:59:01Z","timestamp":1760266741482},"reference-count":43,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T00:00:00Z","timestamp":1132704000000},"content-version":"vor","delay-in-days":9002,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[1981,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Numbers of B cells spontaneously secreting Ig (IgG, IgA, and IgM) were determined by a plaque\u2010forming cell (PFC) assay simultaneously in the peripheral blood and bone marrow of normal individuals, patients with systemic lupus erythematosus (SLE), and patients with primary Sj\u00f6gren's syndrome. Normal individuals had 382 (\u00b1 89) PFC per 10<jats:sup>6<\/jats:sup> mononuclear cells in peripheral blood. Patients with either active or inactive Sj\u00f6gren's syndrome had normal numbers of spontaneous Ig\u2010secreting cells in peripheral blood (<jats:italic>P<\/jats:italic> &gt; 0.2). Conversely, patients with inactive as well as active SLE had markedly increased spontaneous PFC (<jats:italic>P<\/jats:italic> &lt; 0.05 and <jats:italic>P<\/jats:italic> &lt; 0.001, respectively). Patients with active SLE had significantly greater PFC than patients with inactive SLE: 3,984 (\u00b1 960) versus 1,605 (\u00b1 527) PFC per 10<jats:sup>6<\/jats:sup> mononuclear cells (<jats:italic>P<\/jats:italic> &lt; 0.05). The lack of increased numbers of activated B cells in the blood of patients with Sj\u00f6gren's syndrome was not explained by a preferential sequestration of activated B cells in the bone marrow. However, of particular interest was the finding that the bone marrow served not only as a major source of virgin B cells but as a lymphoid organ of either in situ activation of B cells or sequestration for activated B cells. Normal individuals had approximately a 20\u2010fold relative increase of activated B cells per 10<jats:sup>6<\/jats:sup> mononuclear cells in the bone marrow compared to peripheral blood, while patients with inactive and active SLE both had a 35\u2010fold relative increase in activated B cells in bone marrow compared to peripheral blood. The potential relevance of circulating activated B cells and their sequestration in lymphoid organs is discussed concerning the discrepancy in this regard between Sj\u00f6gren's syndrome and SLE, and our understanding of the significance of polyclonal B cell activation in the pathogenesis of these diseases.<\/jats:p>","DOI":"10.1002\/art.1780240402","type":"journal-article","created":{"date-parts":[[2007,2,14]],"date-time":"2007-02-14T19:19:53Z","timestamp":1171480793000},"page":"577-584","source":"Crossref","is-referenced-by-count":82,"title":["Polyclonally triggered B cells in the peripheral blood and bone marrow of normal individuals and in patients with systemic lupus erythematosus and primary sj\u00f6gren's syndrome"],"prefix":"10.1002","volume":"24","author":[{"given":"Anthony S.","family":"Fauci","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haralampos M.","family":"Moutsopoulos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,11,23]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0065-2776(08)60711-7"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9343(59)90037-3"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/00005792-197103000-00001"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-82-3-391"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-91-4-587"},{"key":"e_1_2_1_7_2","first-page":"240","article-title":"Disordered immunologic regulation and autoimmunity","volume":"31","author":"Talal N","year":"1976","journal-title":"Transplant Rev"},{"key":"e_1_2_1_8_2","first-page":"289","article-title":"Animal models of human systemic lupus","volume":"52","author":"Huston DP","year":"1979","journal-title":"Yale J Biol Med"},{"key":"e_1_2_1_9_2","doi-asserted-by":"crossref","first-page":"825","DOI":"10.4049\/jimmunol.120.3.825","article-title":"Delineation of spontaneous erythrocyte autoantibody responses of NZB and other strains of mice","volume":"120","author":"DeHeer DH","year":"1978","journal-title":"J Immunol"},{"key":"e_1_2_1_10_2","doi-asserted-by":"crossref","first-page":"1639","DOI":"10.4049\/jimmunol.119.5.1639","article-title":"Demonstration of activation of B lymphocytes in New Zealand black mice at birth by an immunoradiometric assay for murine IgM","volume":"119","author":"Moutsopoulos HM","year":"1977","journal-title":"J Immunol"},{"key":"e_1_2_1_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/0090-1229(78)90177-0"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.148.5.1198"},{"key":"e_1_2_1_13_2","first-page":"177","volume-title":"Genetic Control of Autoimmunity","author":"Chused TM","year":"1978"},{"key":"e_1_2_1_14_2","first-page":"710","article-title":"Studies of congenitally immunologic mutant: New Zealand mice. 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