Study On The Mechanism Of PSG1-1Engagement Induced The Integrin αLβ2Mediated Leukocyte Adhesion On Fibrinogen

Inflammation is a common and important pathologic process, which is a defense for livingsystem against inflammation factors. Imbalance of inflammation could bring much bad effect.Leukocytes recruitment from blood vessel to inflammation location plays a biological role.The process is regulated by adhesion molecules expressed on leukocyte and endothelial cells.Leukocyte rolling is mediated by selectins and their ligands, the signal could regulate integrinactivation together with chemokines signal.The interaction between activated integrin and itsligands could make leukocyte roll more slowly and mediate firm adhesion to endothelial cells.At last,the leukocyte would transmigrate blood vessel endothelial to inflammation points.PSGL-1is an important selectin ligand expressed on Jurkat cell, a kind of lymphoidlineages. In this article, with the help of cell adhesion assays under static conditions, we foundthat Syk kinase may participate Jurkat cell binding to fibrinogen induced by PSGL-1engagement. According to our immunofluorescence microscopy and flow cytometry data, wedemonstrated that the αLβ2integrin form a cluster on Jurkat cell. Then we found Jurkat cellsrequire intact lipid rafts to mediate adhesion on fibrinogen. When we disrupt lipid rafts withspecial medicine MβCD, the quantity of adherent cells on fibrinogen was dramaticallydecreased. Also the phosphorylation and ability linked with membrance of Syk were evidentlyweaken.