Rolink A G, Brocker T, Bluethmann H, Kosco-Vilbois M H, Andersson J, Melchers F
Basel Institute for Immunology, Switzerland.
Immunity. 1999 May;10(5):619-28. doi: 10.1016/s1074-7613(00)80061-8.
The mature B cell compartment of MHC class II-deficient B6 I-Aalpha(-/-) and the btk-defective CBA/N mouse strain is 4- to 5-fold smaller than in wild-type B6 mice. The defect in B6 I-Aalpha(-/-) mice is intrinsic to B cells and due to a 4- to 5-fold reduced lifespan, which however can be normalized by an I-Ealpha(d) transgene, but only when expressed early during B cell development. The reduced number of mature B cells in the btk-defective CBA/N mouse is due to a 4- to 5-fold lower number of immature splenic B cells entering the mature compartment. The combined defects of reduced lifespan and impaired generation in double mutant mice result in a severe deficiency in the mature B cell pool.
MHC II类缺陷的B6 I-Aα(-/-)小鼠和btk缺陷的CBA/N小鼠品系中成熟B细胞区室比野生型B6小鼠小4至5倍。B6 I-Aα(-/-)小鼠的缺陷是B细胞固有的,并且由于寿命缩短了4至5倍,然而,这可以通过I-Eα(d)转基因来正常化,但前提是在B细胞发育早期表达。btk缺陷的CBA/N小鼠中成熟B细胞数量减少是由于进入成熟区室的未成熟脾B细胞数量减少了4至5倍。双突变小鼠中寿命缩短和生成受损的联合缺陷导致成熟B细胞库严重不足。