Müller W, Kühn R, Rajewsky K
Institute for Genetics, University of Cologne, FRG.
Eur J Immunol. 1991 Apr;21(4):921-5. doi: 10.1002/eji.1830210410.
The murine interleukin 4 (IL4)-encoding cDNA expressed under the control of the immunoglobulin heavy chain enhancer/promoter was inserted into the mouse germ line. All B cells present in the IL4 transgenic mice show a marked increase in expression of class II histocompatibility (Ia) antigens compared to B cells from control mice. In vivo 5-bromo-2'-deoxyuridine incorporation and cell cycle analysis revealed no significant increase in B cell proliferation in spleens of IL4 transgenic mice compared to littermate controls. Likewise, serum immunoglobulin concentrations in IL4 transgenic mice were not increased. From these experiments we conclude that Ia hyperexpression on B cells per se does not induce activation of autoreactive T cells leading to B cell proliferation or hypergammaglobulinemia.
将在免疫球蛋白重链增强子/启动子控制下表达的小鼠白细胞介素4（IL4）编码cDNA插入小鼠种系。与对照小鼠的B细胞相比，IL4转基因小鼠中存在的所有B细胞显示出II类组织相容性（Ia）抗原的表达显著增加。体内5-溴-2'-脱氧尿苷掺入和细胞周期分析显示，与同窝对照相比，IL4转基因小鼠脾脏中的B细胞增殖没有显著增加。同样，IL4转基因小鼠的血清免疫球蛋白浓度也没有增加。从这些实验中我们得出结论，B细胞上的Ia过度表达本身不会诱导自身反应性T细胞的激活，从而导致B细胞增殖或高球蛋白血症。
