ABSTRACT
Aquaporin (AQP)is a molecular weight of about 28 kD of the four polymer structure membrane channel protein. In mammals,there are 1 3 different AQP,expressed in different tissues and organs,regulating waterand glycerol and urea and other small molecules transmembrane transport of major proteins.AQP-1 is mainly expressed in the renal proximal tubule and Henle’s loop drop bronchiole epithelial cell apical membrane and basement membrane,is responsible for the reabsorption of renal tubular water molecules.The expression of AQP-1 can be changed when the kidney is damaged or damaged,so it is very important to study the mechanism of AQP-1 for understanding the pathogenesis of water metabolism and the treatment of clinical water metabolism.
ABSTRACT
Objective To investigate the effects of blockade of OX40/OX40L costimulation pathway on mice islet allograft tolerance in CD40/CD154 costimulation pathway blockade mice.Methods C57BL/6 mice were induced into diabetes mellitus as recipients,and were transplanted with DBA/2 mice islets.The recipients were divided into four groups,(1) treated with IgG as controls,(2) anti-OX40L mAb,(3) anti-CD154,(4) combined treatment of anti-OX40L mAb and anti CD154mAb.The mean survival time (MST) of islet allograft was observed.The expression of OX40 in activated T cells of CD154 deficient mice was detected.Effector T cells were obtained from the spleen of CD154 deficient mice cultured with or without anti-OX40L mAb for 3 days.The proliferation of T cells was assayed.Results The MST in the control group,anti-OX40L mAb group,anti-CD154 mAb group and anti OX40L mAb + anti-CD154 mAb group was 19,22,48,and ＞150 days respectively (P ＜0.05).The OX40 expression was readily induced in the 66％ activated T effector cells.CD154 deficient T effector cells proliferation was inhibited by the addition of anti-OX40L mAb in the culture in a dose-dependent fashion.Conclusion The blockade of OX40/OX40L costimulation pathway can promote islet allograft tolerance in CD40/CD154 costimulation pathway blockade mice by inhibiting the proliferation of T cells.