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A fraction of these cells self-renew and persist as a minor B1 B cell subset throughout life. Here, we show that transfer of early generated B1 B cells from E\u03bc-TCL1 transgenic mice resulted in chronic lymphocytic leukemia (CLL) with a biased repertoire, including stereotyped BCRs. Thus, B1 B cells bearing restricted BCRs can become CLL during aging. Increased anti-thymocyte\/Thy-1 autoreactive (ATA) BCR cells in the B1 B cell subset by transgenic expression yielded spontaneous ATA B-CLL\/lymphoma incidence, enhanced by TCL1 transgenesis. In contrast, ATA B-CLL did not develop from other B cell subsets, even when the identical ATA BCR was expressed on a Thy-1 low\/null background. Thus, both a specific BCR and B1 B cell context were important for CLL progression. Neonatal B1 B cells and their CLL progeny in aged mice continued to express moderately up-regulated c-Myc and down-regulated proapoptotic Bmf, unlike most mature B cells in the adult. Thus, there is a genetic predisposition inherent in B-1 development generating restricted BCRs and self-renewal capacity, with both features contributing to potential for progression to CLL.<\/jats:p>","DOI":"10.1084\/jem.20160712","type":"journal-article","created":{"date-parts":[[2016,11,30]],"date-time":"2016-11-30T15:10:23Z","timestamp":1480518623000},"page":"3007-3024","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":60,"title":["Early generated B1 B cells with restricted BCRs become chronic lymphocytic leukemia with continued c-Myc and low Bmf expression"],"prefix":"10.1084","volume":"213","author":[{"given":"Kyoko","family":"Hayakawa","sequence":"first","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony M.","family":"Formica","sequence":"additional","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joni","family":"Brill-Dashoff","sequence":"additional","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan A.","family":"Shinton","sequence":"additional","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daiju","family":"Ichikawa","sequence":"additional","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yan","family":"Zhou","sequence":"additional","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"III","given":"Herbert C.","family":"Morse","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard R.","family":"Hardy","sequence":"additional","affiliation":[{"name":"Fox Chase Cancer Center, Philadelphia, PA 19111 1"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2016,11,29]]},"reference":[{"key":"2023072603230108400_bib1","doi-asserted-by":"publisher","first-page":"67","DOI":"10.1016\/S1074-7613(01)00257-6","article-title":"CXCL13 is required for B1 cell homing, natural antibody production, and body cavity immunity","volume":"16","author":"Ansel","year":"2002","journal-title":"Immunity."},{"key":"2023072603230108400_bib2","doi-asserted-by":"publisher","first-page":"6955","DOI":"10.1073\/pnas.102181599","article-title":"Human chronic lymphocytic leukemia modeled in mouse by targeted TCL1 expression","volume":"99","author":"Bichi","year":"2002","journal-title":"Proc. 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