Okano Y, Macy M, Harmony J A
Biochim Biophys Acta. 1985 Apr 22;845(1):68-80. doi: 10.1016/0167-4889(85)90056-4.
Plasma lipoproteins of d less than or equal to 1.063 g/ml suppress lymphocyte activation triggered in vitro by polyclonal T cell mitogens. The extent of suppression decreases as the number of accessory cells per culture increases. Accessory cells isolated by glass adherence and by counter-flow centrifugation reduce lipoprotein suppression to the same extent. Modulation of lipoprotein suppression by accessory cells is independent of the amount and type of polyclonal activator. Reduction of lipoprotein suppression requires viable accessory cells and that they be present with lymphocytes, mitogen and lipoproteins during the initial 24-h culture period. It is within this same time period that lipoproteins exert their suppressive effect. Accessory cells isolated from a patient with the homozygous form (receptor-defective) of familial hypercholesterolemia also reduce the extent of lipoprotein suppression, suggesting that modulation is not mediated by the classic low density lipoprotein receptor. There appear to be at least two mechanisms by which accessory cells may alter lipoprotein suppression of T lymphocyte activation: by secretion of a soluble factor, probably not interleukin 1, that decreases the extent of suppression and by direct modification of the population of suppressive lipoproteins. Neither mechanism accounts for the lipoprotein-enhanced activation that occurs when cultures contain approximately equal numbers of T lymphocytes and accessory cells.
密度小于或等于1.063克/毫升的血浆脂蛋白可抑制多克隆T细胞有丝分裂原在体外引发的淋巴细胞活化。随着每个培养物中辅助细胞数量的增加，抑制程度会降低。通过玻璃黏附法和逆流离心法分离的辅助细胞对脂蛋白抑制的降低程度相同。辅助细胞对脂蛋白抑制的调节与多克隆激活剂的数量和类型无关。脂蛋白抑制作用的降低需要有活力的辅助细胞，并且它们在最初的24小时培养期内要与淋巴细胞、有丝分裂原和脂蛋白同时存在。脂蛋白也是在同一时间段内发挥其抑制作用。从家族性高胆固醇血症纯合子形式（受体缺陷型）患者中分离出的辅助细胞也会降低脂蛋白抑制的程度，这表明这种调节不是由经典的低密度脂蛋白受体介导的。辅助细胞改变脂蛋白对T淋巴细胞活化抑制作用的机制似乎至少有两种：通过分泌一种可能不是白细胞介素1的可溶性因子来降低抑制程度，以及通过直接改变抑制性脂蛋白的群体。当培养物中T淋巴细胞和辅助细胞数量大致相等时出现的脂蛋白增强的活化现象，这两种机制都无法解释。
