RESUMO
We report that CD39-expressing-melanoma cells inhibited both T-cell proliferation and the generation of cytotoxic effectors in an adenosine-dependent manner, and that treatment with a CD39-blocking antibody alleviated tumor-mediated immunosuppression. Thus, blocking CD39 ectonucleotidase may represent a novel immunotherapeutic strategy to restore antitumor immunity.
RESUMO
Objective To study the protective effects and mechanisms of adenosine on lung ischemia-reperfusion injury in rabbit. Methods The rabbit ltng model of ischemia-reperfusion was constructed.Thirty Chinese rabbits were random divided into three groups: Group A (no surgery), group B (ischemiareperfusion) and group C (Adenosine + ischemia-reperfusion). The MDA content,SOD content of the plasma, wet-dryrate (W/D) and the pathology of lung tissue and the index of quantitative assessment of histologic lung injury (IQA) were measured after 60 min reperfusion. Results After 60min reperfusion, the value of W/D, MDA and IQA in group B were significantly higher than those in group A (q = 7. 06,13.71,18. 62, P ＜0.01), while the concentration of SOD were lower than those in group A (q = 14. 33, P ＜0.01). In contrast with group B, W/D,MDA and IQA in group C was obviously lower (q =5.23 ,8. 51, 9.99,however, the concentration of SOD were higher than those in group B (q = 7.73, P ＜ 0. 01). In contrast with group A and C ,the expression of CD11b/CD 18 of group B was significantly increased after 60min reperfusion (q =8.59,9.56, P ＜0. 01). Conclusion Adenosine can prevent ischemia-reperfusion injury in rabbit lung in vivo by inhibiting the expression of CD-11b/CD18 on PMNs and dropping oxygen free radicals level.
