Turner M, Gulbranson-Judge A, Quinn M E, Walters A E, MacLennan I C, Tybulewicz V L
National Institute for Medical Research, Mill Hill, London, NW7 1AA, United Kingdom.
J Exp Med. 1997 Dec 15;186(12):2013-21. doi: 10.1084/jem.186.12.2013.
The tyrosine kinase Syk has been implicated as a key signal transducer from the B cell antigen receptor (BCR). We show here that mutation of the Syk gene completely blocks the maturation of immature B cells into recirculating cells and stops their entry into B cell follicles. Furthermore, using radiation chimeras we demonstrate that this developmental block is due to the absence of Syk in the B cells themselves. Syk-deficient B cells are shown to have the life span of normal immature B cells. If this is extended by over-expression of Bcl-2, they accumulate in the T zone and red pulp of the spleen in increased numbers, but still fail to mature to become recirculating follicular B cells. Despite this defect in maturation, Syk-deficient B cells were seen to give rise to switched as well as nonswitched splenic plasma cells. Normally only a proportion of immature B cells is recruited into the recirculating pool. Our results suggest that Syk transduces a BCR signal that is absolutely required for the positive selection of immature B cells into the recirculating B cell pool.
酪氨酸激酶Syk被认为是B细胞抗原受体(BCR)的关键信号转导分子。我们在此表明,Syk基因的突变完全阻断了未成熟B细胞向循环细胞的成熟过程,并阻止它们进入B细胞滤泡。此外,通过辐射嵌合体实验我们证明,这种发育阻滞是由于B细胞自身缺乏Syk所致。研究表明,Syk缺陷型B细胞具有正常未成熟B细胞的寿命。如果通过Bcl-2的过表达来延长其寿命,它们会在脾脏的T区和红髓中数量增加地积聚,但仍无法成熟为循环滤泡B细胞。尽管存在这种成熟缺陷,但仍观察到Syk缺陷型B细胞可产生类别转换和未类别转换的脾浆细胞。通常只有一部分未成熟B细胞被招募进入循环池。我们的结果表明,Syk转导一种BCR信号,该信号对于未成熟B细胞阳性选择进入循环B细胞池是绝对必需的。