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对核因子-κB的p50亚基进行靶向破坏会导致免疫反应出现多灶性缺陷。

Targeted disruption of the p50 subunit of NF-kappa B leads to multifocal defects in immune responses.

作者信息

Sha W C, Liou H C, Tuomanen E I, Baltimore D

机构信息

Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.

出版信息

Cell. 1995 Jan 27;80(2):321-30. doi: 10.1016/0092-8674(95)90415-8.

DOI:10.1016/0092-8674(95)90415-8
PMID:7834752
Abstract

NF-kappa B, a heterodimeric transcription factor composed of p50 and p65 subunits, can be activated in many cell types and is thought to regulate a wide variety of genes involved in immune function and development. Mice lacking the p50 subunit of NF-kappa B show no developmental abnormalities, but exhibit multifocal defects in immune responses involving B lymphocytes and nonspecific responses to infection. B cells do not proliferate in response to bacterial lipopolysaccharide and are defective in basal and specific antibody production. Mice lacking p50 are unable effectively to clear L. monocytogenes and are more susceptible to infection with S. pneumoniae, but are more resistant to infection with murine encephalomyocarditis virus. These data support the role of NF-kappa B as a vital transcription factor for both specific and nonspecific immune responses, but do not indicate a developmental role for the factor.

摘要

核因子-κB(NF-κB)是一种由p50和p65亚基组成的异二聚体转录因子,可在多种细胞类型中被激活,被认为能调控许多参与免疫功能和发育的基因。缺乏NF-κB p50亚基的小鼠未表现出发育异常,但在涉及B淋巴细胞的免疫反应和对感染的非特异性反应中呈现多灶性缺陷。B细胞对细菌脂多糖无增殖反应,且在基础抗体和特异性抗体产生方面存在缺陷。缺乏p50的小鼠无法有效清除单核细胞增生李斯特菌,且更易感染肺炎链球菌,但对鼠脑心肌炎病毒感染更具抵抗力。这些数据支持了NF-κB作为特异性和非特异性免疫反应的重要转录因子的作用,但并未表明该因子在发育过程中的作用。

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