Chou, Wei-ChunWei-ChunChouLevy, David EDavid ELevyCHIEN-KUO LEE2019-07-182019-07-182006-11-010006-4971https://www.scopus.com/inward/record.uri?eid=2-s2.0-33751174311&doi=10.1182%2fblood-2006-05-024430&partnerID=40&md5=4b21fa4a146ff2d27d65625a5f00293dhttps://scholars.lib.ntu.edu.tw/handle/123456789/414293Transcription factors are critical for instructing the development of B lymphocytes from multipotential progenitor cells in the bone marrow (BM). Here, we show that the absence of STAT3 impaired B-cell development. Mice selectively lacking STAT3 in BM progenitor cells displayed reduced numbers of mature B cells, both in the BM and in the periphery. The reduction in the B-cell compartment included reduced percentages and numbers of pro-B, pre-B, and immature B cells in the absence of STAT3, whereas the number of pre-pro-B cells was increased. We found that pro-B and pre-B-cell populations lacking STAT3 were hyporesponsive to IL-7 because of a decreased number of IL-7-responsive cells rather than decreased expression or signaling of IL-7Ralpha. Moreover, STAT3-deficient mice displayed enhanced apoptosis in the pro-B population when deprived of survival factors, suggesting that at least 2 mechanisms (impaired differentiation and enhanced apoptosis) are involved in the mutant phenotype. Last, BM transplantation confirmed that impaired B lymphopoiesis in the absence of STAT3 was caused by a cell autonomous defect. In sum, these studies defined a specific role for STAT3 in early B-cell development, probably acting at the pre-pro-B transition by contributing to the survival of IL-7-responsive progenitors.enjournal article10.1182/blood-2006-05-024430168254892-s2.0-33751174311WOS:000241586100026https://api.elsevier.com/content/abstract/scopus_id/33751174311