{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,31]],"date-time":"2025-10-31T07:15:39Z","timestamp":1761894939288},"reference-count":29,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2009,8,6]],"date-time":"2009-08-06T00:00:00Z","timestamp":1249516800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We recently found that all <jats:italic>trans<\/jats:italic> retinoic acid (ATRA) accelerated B lymphocyte formation. In the current study, we address the question whether retinoids account for the rapid lymphopoiesis that is characteristic of fetal progenitors. Surprisingly, addition of ATRA to fetal liver cultures actually reduced B lymphopoiesis. A pan\u2010retinoid receptor antagonist selectively suppressed lymphocyte formation from fetal and adult progenitors, suggesting some normal contribution of retinoids to this process. Consistent with this role, B lymphopoiesis was compromised in the marrow of mice with prolonged vitamin A deficiency. Recently identified B1 progenitors from adult marrow were similar to adult B2 progenitors in that their differentiation was stimulated by ATRA. The inhibitory response observed with fetal cells was seen when adult progenitors were exposed to high doses in culture or when adult mice were treated with ATRA for 2\u2009wk. In addition to explosive lymphocyte generation, fetal progenitors tend to be less IL\u20107 dependent than their adult counterparts, but ATRA did not make fetal progenitors IL\u20107 independent. We conclude that all known categories of B lineage progenitors are responsive to retinoids and probably regulated by these compounds under physiological conditions. Retinoids may account in part for rapid differentiation in fetal life, but not all unique features of fetal progenitors.<\/jats:p>","DOI":"10.1002\/eji.200939374","type":"journal-article","created":{"date-parts":[[2009,8,6]],"date-time":"2009-08-06T12:32:32Z","timestamp":1249561952000},"page":"2515-2524","source":"Crossref","is-referenced-by-count":13,"title":["A possible contribution of retinoids to regulation of fetal B lymphopoiesis"],"prefix":"10.1002","volume":"39","author":[{"given":"Xinrong","family":"Chen","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert S.","family":"Welner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul W.","family":"Kincade","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2009,8,27]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri2378"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V95.11.3349"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2402625"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.05.014"},{"key":"e_1_2_6_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.leu.2402718"},{"key":"e_1_2_6_7_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.179.5.1665"},{"key":"e_1_2_6_8_2","doi-asserted-by":"crossref","first-page":"58","DOI":"10.4049\/jimmunol.155.1.58","article-title":"All\u2010trans\u2010 and 9\u2010cis\u2010retinoic acid inhibit growth of normal human and murine B cell precursors","volume":"155","author":"Fahlman C.","year":"1995","journal-title":"J. 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