β2整合素亚家族成员LFA-1、Mac-1与配体ICAM-1相互作用虽然均介导炎症级联反应中血流剪切条件下白细胞与血管内皮细胞之间的粘附过程，但是二者却发挥不同生物学功能，前者主要介导慢速滚动与稳定粘附，而后者主要介导爬行。其相应作用机制尚不明确。本项目围绕LFA-1、Mac-1功能差异的分子作用机制这一科学问题，结合生物力学与分子动力学模拟手段，开展以下研究：1）定量比较力学因素对LFA-1-ICAM-1、Mac-1-ICAM-1相互作用反应动力学的调控规律；2）模拟预测LFA-1、Mac-1微观结构动力学差异性。采用模拟预测、实验定量测量以及验证模拟的研究思路为深入认识LFA-1、Mac-1的结构-功能关系提供基础数据，并为未来药物设计提供新线索。

Both LFA-1-ICAM-1 and Mac-1-ICAM-1 interactions modulate the adhesion between leukocyte and endothelium under blood flow in inflammation cascade, while they play distinct roles with the former involving in slow rolling and firm adhesion and the latter mediating the crawling, and the corresponding molecular mechanism remains unclear. The scientific issue of this project focuses on investigating the molecular mechanism for elucidating the different function between LFA-1 and Mac-1. With the combination of biomechanical technology and molecular dynamics simulations, the scientific aims include: 1) Quantify the impact of external force on the binding kinetics of LFA-1-ICAM-1 and Mac-1-ICAM-1 interactions; 2) Predict the dynamic features of micro-structures of LFA-1 and Mac-1. Upon the research approach of simulation predicting experiment and experiment approving simulation, the goal of this project is to deepen the understanding of structure-function relationship of LFA-1 and Mac-1, and to offer new insight into drug design.