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细胞通过低密度脂蛋白受体（ＬＤＬ－Ｒ）介导的ＬＤＬ内吞及自身合成而保持胞内胆固醇的平衡。本研究以人工脂双层膜与人外周血淋巴细胞孵育，将外源性胆固醇导入细胞内，同时用ＨＭＧ－ＣｏＡ还原酶抑制剂抑制内源性胆固醇合成。结果显示，随细胞胆固醇含量升高，有丝分裂期细胞增多，细胞增殖转化能力增强。用Ｌｏｖａｓ－ｔａｔｉｎ抑制内源性胆固醇合成，淋巴细胞大部分受阻于Ｇ０／Ｇ１期，细胞增殖活性降低，且这种抑制作用不能被外源性重组ＩＬ－２所逆转。膜胆固醇过高，淋巴细胞功能反而降低。淋巴细胞活化中期标志物ＣＤ７１分子在膜上的表达及其与配体的结合容量也受细胞胆固醇含量调节。
Cells maintain intracellular cholesterol balance by LDL-R mediated endocytosis of LDL and its own synthesis. In this study, artificial bilayer membranes incubated with human peripheral blood lymphocytes, exogenous cholesterol into cells, while using HMG-CoA reductase inhibitors inhibit endogenous cholesterol synthesis. The results showed that with the increase of cellular cholesterol, mitotic cells increased, cell proliferation and transformation ability increased. Lovas-tatin inhibited endogenous cholesterol synthesis, most of the lymphocytes blocked in the G0 / G1 phase, cell proliferation decreased, and this inhibition can not be reversed by exogenous recombinant IL-2. Membrane cholesterol is too high, but lower lymphocyte function. The expression of the CD71 molecule on the membrane of lymphocyte activation metaphase and its binding capacity to the ligand are also regulated by the cellular cholesterol content.