{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T00:28:23Z","timestamp":1789950503826,"version":"4.0.1"},"reference-count":69,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2000,2,1]],"date-time":"2000-02-01T00:00:00Z","timestamp":949363200000},"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":[[2000,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Phenotypic analysis of bone marrow cells from IL-7 knockout (KO) mice revealed that B cell development is blocked precisely at the transition between pro-B cells and pre-B cells. In contrast, the generation of pre-pro-B cells and pro-B cells appeared to be normal, as judged by total cell numbers, proliferative indexes, D-JH and V-DJH gene rearrangements, and mRNA for recombinase-activating gene-1 (RAG-1), RAG-2, TdT, Ig\u03bc, \u03bb5, and VpreB. However, upon closer inspection, several abnormalities in pro-B cell development were identified that could be corrected by injection of rIL-7 in vivo. These included the absence of the subset of late pro-B cells that initiates c\u03bc expression for pre-B cell Ag receptor (BCR) formation, and the failure of pro-B cells to up-regulate TdT and the IL-7R\u03b1 (but not the common \u03b3-chain) chain. Similar defects were present in common \u03b3-chain and Jak3 KO mice, but not in \u03bb5 or (excluding cytoplasmic Ig \u03bc heavy chain (c\u03bc)) RAG-1 KO mice, all of which also arrest at the late pro-B cell stage. Consequently, up-regulation of TdT and IL-7R\u03b1 expression requires signaling through the high affinity IL-7R, but does not require c\u03bc expression or a functional pre-BCR. Taken together, these results suggest that IL-7 and its receptor complex are essential for 1) up-regulating the expression of TdT and IL-7R\u03b1, 2) initiating the production of c\u03bc, and 3) promoting the formation of a functional pre-BCR in\/on pro-B cells. These key events, in turn, appear to be prerequisite both for differentiation of pro-B cells to pre-B cells and for proliferation of these cell subsets upon continued stimulation with IL-7.<\/jats:p>","DOI":"10.4049\/jimmunol.164.4.1961","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T14:44:52Z","timestamp":1398177892000},"page":"1961-1970","source":"Crossref","is-referenced-by-count":58,"title":["Murine Pro-B Cells Require IL-7 and Its Receptor Complex to Up-Regulate IL-7R\u03b1, Terminal Deoxynucleotidyltransferase, and c\u03bc Expression"],"prefix":"10.1093","volume":"164","author":[{"given":"Chiju","family":"Wei","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Connecticut Health Center , Farmington, CT 06030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Zeff","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Connecticut Health Center , Farmington, CT 06030"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irving","family":"Goldschneider","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Connecticut Health Center , Farmington, CT 06030"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,2,15]]},"reference":[{"key":"2026020213173460400_R1","first-page":"988","volume-title":"J. 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