Contribution of monocytes Siglec-1 in stimulating T cells proliferation and activation in atherosclerosis
Contribution of monocytes Siglec-1 in stimulating T cells proliferation and activation in atherosclerosis
复制标题
单核细胞 Siglec-1 在刺激动脉粥样硬化 T 细胞增殖和活化中的作用
DOI：
10.1016/j.atherosclerosis.2012.06.063
复制
发表时间：
2012-09-01
期刊：
影响因子：
5.3
通讯作者：
Zhong, Ren-qian
中科院分区：
文献类型：
--
作者：
Xiong, Yi-song;Wu, Ai-lin;Zhong, Ren-qian
Objective: Atherosclerosis (AS) is widely accepted as an inflammatory disease and monocytes are particularly important in inflammatory immune responses. As an important biomarker of monocytes activation, Siglec-1 is highly expressed on circulating monocytes and atherosclerotic plaques of coronary artery disease (CAD) patients, but the exact role of Siglec-1 has not been elucidated.Methods: M-CSF, INF-alpha, IFN-gamma, TNF-alpha and ox-LDL alone or in combination were used to stimulate Siglec-1 expression on monocytes, whereas small interfering RNA (si-RNA) or blocking antibody was used to down-regulate Siglec-1. Meanwhile, the role of Siglec-1 in chemokines secretion was determined. Then monocytes from CAD patients or healthy controls were cocultured with CD4+ or CD8+ T cells from a third healthy individual, and lymphocyte proliferation and activation were determined.Results: All the stimuluses could enhance Siglec-1 expression on monocytes in a dose-dependent manner, and M-CSF could synergistically stimulate Siglec-1 expression with ox-LDL. Moreover, the secretion of MCP-1, MIP-1 alpha and MIP-2 were enhanced when Siglec-1 was up-regulated and down to normal level when Siglec-1 was blocked. More importantly, increased Siglec-1 expression on monocytes was related to the increased T cell proliferation and pro-inflammatory cytokines secretion in CAD patients. However, down-regulation of Siglec-1 could attenuate proliferation and activation of cocultured CD4+ and CD8+ T cells.Conclusion: Siglec-1 can promote chemokines and pro-inflammatory cytokines secretion and influence the inflammatory process of AS. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
