Baixeras E, Moreno M C, Martinez-A C
Centro Nacional de Biotecnologia (C.S.I.C), Universidad de Madrid, Spain.
Cell Immunol. 1996 Jul 10;171(1):55-61. doi: 10.1006/cimm.1996.0172.
We have described recently the prevention of apoptosis by CD2-soluble CD48 interaction on antigen B cell receptor occupancy. Here, we show that CD2 ligation is also able to interfere with B cell receptor-independent apoptosis pathways such as spontaneous death in spleen B cells or serum deprivation and hydrogen peroxide exposure in the BAL-17 cell line. In all cases, CD2 ligation induces a signal that prevents the downregulation of Bcl-2 expression. The specific CD2 signal pathway involved in this phenomenon is still unknown. As reported, CD2 did not appear to induce Ca2+ mobilization, phosphatidylinositol turnover, or PKC translocation in B cells. Nevertheless, we show that CD2 receptor ligation is coupled to the tyrosine phosphorylation pathway in B cells. These observations indicate that CD2 is functionally able to trigger at least an early signal that could play a role in apoptosis blockage B cells in addition to the adhesion one. The results suggest the participation of cellular membrane receptors other that CD40 in apoptosis rescue, not only in the antigen-dependent but also in the antigen-independent phases of B cell lymphopoiesis.
我们最近描述了抗原B细胞受体占据时CD2-可溶性CD48相互作用对细胞凋亡的预防作用。在此,我们表明CD2连接还能够干扰不依赖B细胞受体的凋亡途径,如脾脏B细胞中的自然死亡或BAL-17细胞系中的血清剥夺和过氧化氢暴露。在所有情况下,CD2连接都会诱导一个信号,阻止Bcl-2表达的下调。参与这一现象的特定CD2信号通路仍然未知。如前所述,CD2似乎不会在B细胞中诱导Ca2+动员、磷脂酰肌醇周转或PKC易位。然而,我们表明CD2受体连接与B细胞中的酪氨酸磷酸化途径相关。这些观察结果表明,CD2在功能上能够触发至少一个早期信号,除了黏附信号外,该信号可能在B细胞凋亡阻滞中发挥作用。结果表明,除CD40外的细胞膜受体参与了凋亡挽救,不仅在B细胞淋巴细胞生成的抗原依赖阶段,而且在抗原非依赖阶段。