{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,25]],"date-time":"2026-04-25T15:29:19Z","timestamp":1777130959945,"version":"3.51.4"},"reference-count":17,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,12,6]],"date-time":"2005-12-06T00:00:00Z","timestamp":1133827200000},"content-version":"vor","delay-in-days":6124,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1989,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Studies presented here, conducted with allotype homozygotes, demonstrate the existence of a feedback mechanism that regulates development of Ly\u20101 B cells from immature progenitors. In the preceding study (P. A. Lalor et al., <jats:italic>Eur. J. Immunol.<\/jats:italic> 1989. <jats:italic>19<\/jats:italic>: 501), conducted with allotype heterozygotes, we showed that treating neonates with monoclonal antibody to the paternal allotype IgM depletes roughly half of the neonatal B cell population (<jats:italic>i.e.<\/jats:italic> those expressing the paternal IgM allotype) and that paternal allotype Ly\u20101 B cells specificically remain depleted for the life of the animal. Here we show that treating allotype homozygotes with the same antibody depletes all (rather than half) of the B cells and that, under these conditions, relatively normal numbers of Ly\u20101 B cells reappear shortly after the treatment antibody disappears. This recovery, we also show, is prevented by restoring allotype\u2010congenic Ly\u20101 B cells to the treated homozygotes, <jats:italic>i.e.<\/jats:italic> by reconstituting treated neonates with allotype\u2010congenic peritoneal cells, sorted Ly\u20101 B cells or a monoclonal population of Ly\u20101 B \u201ctumor\u201d cells.<\/jats:p><jats:p>These findings in essence reveal a feedback mechanism through which mature Ly\u20101 B cells prevent further Ly\u20101 B cell development from Ig<jats:sub>\u2010<\/jats:sub> precursors. This feedback regulation is independent of Ig secretion by the mature Ly\u20101 B cells, since the monoclonal Ly\u20101 B \u201ctumor\u201d population that prevents endogenous Ly\u20101 B development does not secrete Ig. Furthermore, it appears to be independent of Ly\u20101 B surface Ig specificity, since a monoclonal population is sufficient to block all Ly\u20101 B cell development. This mechanism appears to operate normally to fix the composition of the Ly\u20101 B population, which survives through self\u2010replenishment in adults, in accord with conditions that influence Ly\u20101 B development during neonatal life.<\/jats:p>","DOI":"10.1002\/eji.1830190315","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T10:36:36Z","timestamp":1172745396000},"page":"507-513","source":"Crossref","is-referenced-by-count":130,"title":["Feedback regulation of murine Ly\u20101 B cell development"],"prefix":"10.1002","volume":"19","author":[{"given":"Paul A.","family":"Lalor","sequence":"first","affiliation":[]},{"given":"Leonore A.","family":"Herzenberg","sequence":"additional","affiliation":[]},{"given":"Sharon","family":"Adams","sequence":"additional","affiliation":[]},{"given":"Alan M.","family":"Stall","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2005,12,6]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830190314"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830091104"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830110406"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830110408"},{"key":"e_1_2_1_6_2","doi-asserted-by":"crossref","first-page":"787","DOI":"10.4049\/jimmunol.132.2.787","volume":"132","author":"Stall A. M.","year":"1984","journal-title":"J. Immunol."},{"key":"e_1_2_1_7_2","unstructured":"Stall A. M. Farinas M. C. Tarlinton D. M. Lalor P. A. Strober S. Herzenberg L. A.andHerzenberg L. A. Proc. Natl. Acad. Sci. 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