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Transgenic mice deficient in <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>13 or its receptor <jats:styled-content style=\"fixed-case\">CXCR<\/jats:styled-content>5 have severely impaired lymph node development, lack peritoneal B\u2010lymphocytes and are deficient in circulating antibodies to common bacterial antigens. However, total circulating numbers of B\u2010lymphocytes are slightly elevated and humoral responses to T\u2010dependent or blood\u2010borne antigens are relatively normal. Lymphoid neogenesis is an aberrant process that occurs in chronically inflamed tissue and provides a microenvironment supportive of pathogenic B\u2010cell survival and activation. Here, we describe the impact of therapeutic dosing of a <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>13 antibody in a mouse model of arthritis, and detail the contribution <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>13 makes to lymphoid follicle microenvironment, without affecting humoral immune responses.<\/jats:p>","DOI":"10.1111\/eci.12063","type":"journal-article","created":{"date-parts":[[2013,2,8]],"date-time":"2013-02-08T13:06:37Z","timestamp":1360328797000},"page":"501-509","source":"Crossref","is-referenced-by-count":73,"title":["Effects of <scp>CXCL<\/scp>13 inhibition on lymphoid follicles in models of autoimmune disease"],"prefix":"10.1111","volume":"43","author":[{"given":"Donna K.","family":"Finch","sequence":"first","affiliation":[{"name":"MedImmune Ltd Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel","family":"Ettinger","sequence":"additional","affiliation":[{"name":"MedImmune LLC 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