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在缺乏蛋白质激酶Cdelta的小鼠中增加了B细胞的增殖和自身免疫

Akimoto Miyamoto¹, Keiko Nakayama, Hiroyuki Imaki

¹Department of Molecular and Cellular Biology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.

|April 27, 2002

概括

蛋白激酶C-delta (PKC-delta) 通常会抑制B细胞的增殖. 缺乏PKC-delta的小鼠表现出不受控制的B细胞生长,这表明它在维持免疫耐受性方面发挥着至关重要的作用.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

蛋白激酶C (PKC) 异型调节各种细胞功能,包括生长和亡.
在PKC异型中,PKC-delta因其细胞生长抑制特性而独一无二.
在B淋巴细胞调节和免疫耐受性中PKC-delta的作用尚未完全理解.

研究的目的:

研究PKC-delta在B淋巴细胞发育和调节中的作用.
确定PKC-delta缺乏对B细胞增殖和免疫耐受性的影响.

主要方法:

产生和分析缺乏PKC-delta的小鼠.
评估B-淋巴细胞种群和生殖中心的形成.
来自野生型和PKC-delta-null小鼠的B细胞的体外增殖试验.
收养转移实验以评估B细胞自主效应.
分析介质素-6 (IL-6) 的产生和NF-IL6的DNA结合活性.
评估自身抗体,凝聚甲状腺炎和器官透.

主要成果:

缺乏PKC-delta的小鼠表现出B淋巴细胞和生殖中心的自发扩张.
来自PKC-delta-null小鼠的B细胞在刺激时表现出高增殖.
超增殖表型是B细胞固有的.
在缺乏PKC-delta的B细胞中增加IL-6的产生与增强的NF-IL6DNA结合活性有关.
缺少PKC-delta的小鼠会产生自身抗体,质炎和器官透.

结论:

PKC-delta在B细胞增殖的负调节中起着至关重要的作用.
PKC-delta对于建立和维持B细胞耐受性至关重要.
失去PKC-delta会导致自身免疫表现,原因是B细胞过度增殖和耐受性丧失.

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