{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T07:10:58Z","timestamp":1770102658136,"version":"3.49.0"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2005,8,1]],"date-time":"2005-08-01T00:00:00Z","timestamp":1122854400000},"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":[[2005,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Fc\u03b3RIIB, a low-affinity FcR for IgG, inhibits BCR-mediated activation when these two receptors are cocross-linked by Ags and IgG-containing immune complexes. Although a role for Fc\u03b3RIIB in the germinal center (GC) reaction has been proposed, conflicting results have been published regarding the levels of Fc\u03b3RIIB expressed on GC B cells in normal and autoimmune-prone mice and humans. In the present study, we investigate this issue in detail in mice by using multiple GC B cell markers, two different antigenic systems, primary and secondary GC responses, and by excluding the influence of splenic influx of immature B cells and passive acquisition of Fc\u03b3RIIB from follicular dendritic cells. Our results are in concordance with previous data indicating that Fc\u03b3RIIB expression is up-regulated on GC B cells in normal mice. In contrast, we observe comparable levels of Fc\u03b3RIIB on GC and non-GC B cells in New Zealand White, New Zealand Black, and B6.Sle1 autoimmune-prone strains. Therefore, we suggest that these strains exhibit failed up-regulation of Fc\u03b3RIIB on GC B cells, rather than down-regulation, as previously suggested. Also, in contrast to previous indications, this perturbed regulation is not uniquely associated with deletion polymorphisms in the promoter region of the Fc\u03b3RIIB gene but does appear to be independent of genetic background. Finally, we present evidence indicating that Fc\u03b3RIII, a low-affinity activating IgG FcR, is expressed on the GC B cells of normal but not autoimmune-prone mice.<\/jats:p>","DOI":"10.4049\/jimmunol.175.3.1440","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T23:20:32Z","timestamp":1398036032000},"page":"1440-1449","source":"Crossref","is-referenced-by-count":28,"title":["Failed Up-Regulation of the Inhibitory IgG Fc Receptor Fc\u03b3RIIB on Germinal Center B Cells in Autoimmune-Prone Mice Is Not Associated with Deletion Polymorphisms in the Promoter Region of the\n                    <i>Fc<\/i>\n                    \u03b3\n                    <i>RIIB<\/i>\n                    Gene"],"prefix":"10.1093","volume":"175","author":[{"given":"Ziaur S M","family":"Rahman","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology and Kimmel Cancer Center, Jefferson Medical College , Philadelphia, PA 19107"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tim","family":"Manser","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology and Kimmel Cancer Center, Jefferson Medical College , Philadelphia, PA 19107"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,8,1]]},"reference":[{"key":"2026020214053903200_R1","first-page":"1","volume-title":"Adv. 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