{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,3,27]],"date-time":"2025-03-27T09:40:04Z","timestamp":1743068404500,"version":"3.40.3"},"reference-count":29,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2012,4,1]],"date-time":"2012-04-01T00:00:00Z","timestamp":1333238400000},"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":[[2012,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Calcium-modulating cyclophilin ligand (CAML) is a ubiquitously expressed protein that is important during thymopoiesis. However, whether it serves a function in mature lymphocytes is unknown. In this article, we show that CAML is essential for survival of peripheral follicular (Fo) B cells. Conditional deletion of CAML in CD19-Cre transgenic mice caused a significant reduction in Fo cell numbers and increased rates of homeostatic proliferation. CAML-deficient Fo cells showed increased cellular turnover and normal proliferative ability. Although CAML-deficient Fo cells responded to AgR stimulation and to B cell activating factor, they displayed decreased survival and increased apoptosis following stimulation with LPS and IL-4 in vitro. Failure to survive was not due to aberrant B cell development in the absence of CAML, because induced deletion of the gene in mature cells resulted in a similar phenotype. These data establish an essential and ongoing role for CAML in the long-term survival of mature B cells.<\/jats:p>","DOI":"10.4049\/jimmunol.1101641","type":"journal-article","created":{"date-parts":[[2012,2,21]],"date-time":"2012-02-21T03:46:54Z","timestamp":1329796014000},"page":"3009-3018","source":"Crossref","is-referenced-by-count":7,"title":["Essential Role for CAML in Follicular B Cell Survival and Homeostasis"],"prefix":"10.1093","volume":"188","author":[{"given":"Nicholas A","family":"Zane","sequence":"first","affiliation":[{"name":"Department of Immunology, College of Medicine , Mayo Clinic, Rochester, MN 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Justin H","family":"Gundelach","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Adolescent Medicine, College of Medicine , Mayo Clinic, Rochester, MN 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lonn D","family":"Lindquist","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Adolescent Medicine, College of Medicine , Mayo Clinic, Rochester, MN 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard J","family":"Bram","sequence":"additional","affiliation":[{"name":"Department of Immunology, College of Medicine , Mayo Clinic, Rochester, MN 55905"},{"name":"Department of Pediatrics and Adolescent Medicine, College of Medicine , Mayo Clinic, Rochester, MN 55905"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2012,4,1]]},"reference":[{"key":"2025032409595154800_r1","doi-asserted-by":"crossref","first-page":"1213","DOI":"10.1084\/jem.173.5.1213","article-title":"Resolution and characterization of pro-B and pre-pro-B cell stages in normal mouse bone marrow","volume":"173","author":"Hardy","year":"1991","journal-title":"J. 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