Morikawa K, Oseko F, Morikawa S
Department of Internal Medicine, Shimane Medical University, Japan.
Transplantation. 1992 Dec;54(6):1025-30. doi: 10.1097/00007890-199212000-00016.
We examined the effect of FK506 on the activation, proliferation and differentiation of human B lymphocytes in vitro. FK506 inhibited the proliferative response of resting B cells induced by Staphylococcus aureus Cowan strain I (SAC) and phorbol myristate acetate (PMA) in a dose-dependent manner. Inhibition of cell proliferation by FK506 was caused by a selective block of G0 to G1 phase transition leading to cell arrest. In addition, the proliferative response of in vivo-activated B cells and lymphokine-driven B cell proliferation were also found to be sensitive to FK506. Interestingly, FK506 did not affect the expression of activation antigens such as CD23, IL-2 receptor (CD25), and transferrin receptor (CD71). Finally, FK506 had little effect on B cell antibody generation in a T cell-independent system. Conversely, FK506 suppressed neither proliferation nor immunoglobulin secretion in a human B lymphoblastoid cell line. These results indicate that FK506 has discrete effects on the different stages of the B cell maturation.
我们在体外研究了FK506对人B淋巴细胞激活、增殖和分化的影响。FK506以剂量依赖的方式抑制了金黄色葡萄球菌考恩I株（SAC）和佛波酯（PMA）诱导的静息B细胞的增殖反应。FK506对细胞增殖的抑制是由于选择性阻断G0到G1期的转变导致细胞停滞。此外，还发现体内激活的B细胞的增殖反应和细胞因子驱动的B细胞增殖对FK506敏感。有趣的是，FK506不影响激活抗原如CD23、白细胞介素-2受体（CD25）和转铁蛋白受体（CD71）的表达。最后，FK506在非T细胞依赖系统中对B细胞抗体产生几乎没有影响。相反，FK506既不抑制人B淋巴母细胞系的增殖，也不抑制免疫球蛋白的分泌。这些结果表明FK506对B细胞成熟的不同阶段有不同的作用。
