Pax5/BSAP maintains the identity of B cells in late B lymphopoiesis

被引:208
作者
Horcher, M [1 ]
Souabni, A [1 ]
Busslinger, M [1 ]
机构
[1] Res Inst Mol Pathol, Vienna Bioctr, A-1030 Vienna, Austria
关键词
D O I
10.1016/S1074-7613(01)00153-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The a lineage commitment factor Pax5 (BSAP) is expressed throughout B cell development. To investigate its late function, we generated a mouse strain carrying a flexed Pax5 allele that was conditionally inactivated by CD19-cre or Mx-cre expression. Pax5 deletion resulted in the preferential loss of mature B cells, inefficient lymphoblast formation, and reduced serum IgG levels. Mature B cells radically changed their gene expression pattern in response to Pax5 inactivation. Most B cell antigens were downregulated on the cell surface, and the transcription of B cell-specific genes was decreased, whereas the expression of non-B lymphoid genes was activated in Pax5-deficient B cells. These data demonstrate that Pax5 is essential for maintaining the identity and function of B cells during late B lymphopoiesis.
引用
收藏
页码:779 / 790
页数:12
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