免疫學研究所CHOU, WEI-CHUNWEI-CHUNCHOULEE, CHIEN-KUOCHIEN-KUOLEE周威君李建國2011-04-292018-07-092011-04-292018-07-092006-11http://ntur.lib.ntu.edu.tw//handle/246246/233064Transcription 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-7R alpha . 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 lymphopolesis 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.371739 bytesapplication/pdfen-UShttp://ntur.lib.ntu.edu.tw/bitstream/246246/233064/1/Blood 2006.pdf