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八聚体转录因子2(Oct-2)基因缺失可消除腹膜B-1淋巴细胞谱系,并减弱B-2细胞的成熟和功能。

oct-2 gene disruption eliminates the peritoneal B-1 lymphocyte lineage and attenuates B-2 cell maturation and function.

作者信息

Humbert P O, Corcoran L M

机构信息

Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139, USA.

出版信息

J Immunol. 1997 Dec 1;159(11):5273-84.

PMID:9548466
Abstract

Targeted mutation of the gene for the Oct-2 transcription factor in mice caused neonatal lethality and abrogated mitogen-induced proliferation and differentiation of mature B lymphocytes in vitro. Here we show that Oct-2 is required for normal humoral responses upon immunization with T cell-dependent as well as T-independent Ags. oct-2-null T cell behavior was normal, implying a B cell-restricted lesion. oct-2-/- B cells displayed aberrant behavior during activation in vitro: both acquisition of markers of cellular activation and cell survival were diminished. Production of early B lineage cells in the bone marrow was normal, yet mature B cells were under-represented in blood and lymphoid organs. Furthermore, peritoneal B-1 lymphocytes were not detected in animals with a reconstituted oct-2-/- lymphoid system. We conclude that Oct-2 is required for B-1 cell maintenance and for normal Ag-driven maturation of conventional B cells in vivo.

摘要

小鼠中Oct-2转录因子基因的靶向突变导致新生期致死,并在体外消除了有丝分裂原诱导的成熟B淋巴细胞的增殖和分化。在此我们表明,在用T细胞依赖性以及T细胞非依赖性抗原免疫时,Oct-2是正常体液反应所必需的。Oct-2基因敲除小鼠的T细胞行为正常,这意味着是B细胞特异性损伤。Oct-2基因敲除的B细胞在体外激活过程中表现出异常行为:细胞激活标志物的获得和细胞存活均减少。骨髓中早期B谱系细胞的产生正常,但血液和淋巴器官中成熟B细胞的比例不足。此外,在重建了Oct-2基因敲除淋巴系统的动物中未检测到腹膜B-1淋巴细胞。我们得出结论,Oct-2是体内B-1细胞维持以及传统B细胞正常抗原驱动成熟所必需的。

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