Bijsterbosch M K, Klaus G G
Immunology. 1985 Nov;56(3):435-40.
The degradation of phosphatidylinositol bisphosphate (PIP2) to diacylglycerol and inositol trisphosphate is elicited by ligand-receptor interactions in many cell types, and may be involved in the induction of cell growth. The mitogens concanavalin A and anti-immunoglobulin antibodies have previously been shown to induce degradation of PIP2 in mouse thymocytes and B cells, respectively. We have now investigated the effects of the immunosuppressive peptide cyclosporine (CS) on this response, since CS appears to inhibit an early step in lymphocyte activation by mitogens that induce PIP2 degradation and Ca2+ mobilization. We found that CS, at doses that completely abrogated the proliferative responses, did not affect the degradation of inositol phospholipids in either thymocytes or B cells. We therefore conclude that if PIP2 degradation is implicated in lymphocyte activation, then CS does not interfere with the second messenger production initiated by PIP2 breakdown, but rather with a later event(s) elicited by this pathway.
在许多细胞类型中，磷脂酰肌醇二磷酸（PIP2）降解为二酰基甘油和肌醇三磷酸是由配体-受体相互作用引发的，并且可能参与细胞生长的诱导。促有丝分裂原伴刀豆球蛋白A和抗免疫球蛋白抗体先前已分别被证明可诱导小鼠胸腺细胞和B细胞中PIP2的降解。我们现在研究了免疫抑制肽环孢素（CS）对这种反应的影响，因为CS似乎抑制了由诱导PIP2降解和Ca2+动员的促有丝分裂原引起的淋巴细胞激活的早期步骤。我们发现，在完全消除增殖反应的剂量下，CS不会影响胸腺细胞或B细胞中肌醇磷脂的降解。因此，我们得出结论，如果PIP2降解与淋巴细胞激活有关，那么CS不会干扰由PIP2分解引发的第二信使产生，而是干扰该途径引发的后续事件。
