Abstract:Aim To study the correlations between the proportion and GM1 levels of lymphocyte subsets as well as cell activation and serum cholesterol levels and to discuss how high levels of cholesterol regulate lymphocyte functions and the relations to atherosclerosis. Methods A total of sixty subjects were randomly enrolled in this study during their regular physical examination with thirty females and thirty males, aged between 60 and 80 years. The proportions of peripheral blood total B lymphocytes(CD19+), naive B cells(CD19+CD27-), memory B cells(CD19+CD27+), total T lymphocytes(CD3+), CD3+CD4+ and CD3+CD8+ T cells and their expression of GM1 were determined by antibody staining and flow cytometry. Phosphorylated Stat3 was detected by intracellular staining. The results were analyzed with respect of their correlations with serum cholesterol levels and the occurrence of arthrosclerosis. Results The proportion of CD19+ total B cells and low density lipoprotein cholesterol(LDLC)levels as well as the proportion of CD19+CD27+ memory B cells and very low density lipoprotein cholesterol(VLDLC)levels showed significantly positively correlations(P<0.05). We have not found any significant correlations between T cell subsets and cholesterol levels(P>0.05). The GM1 levels of memory B cells were positively correlated with both total cholesterol(TC)levels and VLDLC levels(P<0.05). The GM1 levels of CD3+CD8+ cells were positively correlated with high density lipoprotein cholesterol(HDLC)levels(P<0.05). BCR stimulation induced activation of Stat3. There was significant increase in the levels of Stat3 phosphorylation in high-cholesterol group compared with low-cholesterol group(P<0.01). Conclusions High cholesterol level is a major risk factor for atherosclerosis in the elderly. The correlations between the high cholesterol levels and the proportion, GM1 levels of lymphocyte subsets and Stat3 activation suggested high cholesterol levels may regulate lymphocyte proliferation, activation, proinflammatory cytokine production, and thus promote atherosclerosis.