{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:00:13Z","timestamp":1791295213058,"version":"4.1.0"},"reference-count":0,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1993,1,1]]},"abstract":"<jats:p>To assess the role of immunoglobulin D (IgD) in vivo we generated IgD-deficient mice by gene targeting and studied B cell development and function in the absence of IgD expression. In the mutant animals, conventional and CD5-positive (B1) B cells are present in normal numbers, and the expression of the surface markers CD22 and CD23 in the compartment of conventional B cells indicates acquisition of a mature phenotype. As in wild-type animals, most of the peripheral B cells are resting cells. The IgD-deficient mice respond well to T cell-independent and -dependent antigens. However, in heterozygous mutant animals, B cells expressing the wild type IgH locus are overrepresented in the peripheral B cell pool, and T cell-dependent IgG1 responses are further dominated by B cells expressing the wild-type allele. Similarly, in homozygous mutant (IgD-deficient) animals, affinity maturation is delayed in the early primary response compared to control animals, although the mutants are capable of generating high affinity B cell memory. Thus, rather than being involved in major regulatory processes as had been suggested, IgD seems to function as an antigen receptor optimized for efficient recruitment of B cells into antigen-driven responses. The IgD-mediated acceleration of affinity maturation in the early phase of the T cell-dependent primary response may confer to the animal a critical advantage in the defense against pathogens.<\/jats:p>","DOI":"10.1084\/jem.177.1.45","type":"journal-article","created":{"date-parts":[[2004,6,24]],"date-time":"2004-06-24T07:56:10Z","timestamp":1088063770000},"page":"45-55","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":190,"title":["Immunoglobulin D (IgD)-deficient mice reveal an auxiliary receptor function for IgD in antigen-mediated recruitment of B cells."],"prefix":"10.1084","volume":"177","author":[{"given":"J","family":"Roes","sequence":"first","affiliation":[{"name":"Institute for Genetics, University of Cologne, FRG."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K","family":"Rajewsky","sequence":"additional","affiliation":[{"name":"Institute for Genetics, University of Cologne, FRG."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[1993,1,1]]},"container-title":["The Journal of experimental medicine"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/177\/1\/45\/1674129\/45.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/rupress.org\/jem\/article-pdf\/177\/1\/45\/1674129\/45.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,7,25]],"date-time":"2023-07-25T04:51:13Z","timestamp":1690260673000},"score":1,"resource":{"primary":{"URL":"https:\/\/rupress.org\/jem\/article\/177\/1\/45\/24650\/Immunoglobulin-D-IgD-deficient-mice-reveal-an"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1993,1,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1993,1,1]]}},"URL":"https:\/\/doi.org\/10.1084\/jem.177.1.45","relation":{},"ISSN":["0022-1007","1540-9538"],"issn-type":[{"value":"0022-1007","type":"print"},{"value":"1540-9538","type":"electronic"}],"subject":[],"published":{"date-parts":[[1993,1,1]]}}}