Radiation Therapy For B7-H1and Immune Escape Of Glioma Cells

Radiation is one of the comprehensive treatment for the nervous tumors especiallyglioma,it can prolong the survival time of patient from six to eight months on average, but therecurrence rate is still more than90%even after radiation therapy. It plays a very important roleof the tumor cells which escape from immune surveillance of the host. Now it is unclear thatwhat the radiation therapy do on tumor tissue of the inherent escape. In recent years, the hotpoint of immune escape and cell surface molecules is molecular B7family, including B7-H1.B7-H1is also known as programmed death ligand-1(PD-L1), its genes has been identifiedon a region of chromosome9, The open reading frame of the B7-H1gene encodes a putativetype I transmembrane protein of290amino acids, consisting of immunoglobulin V-like and C-like domains, a hydrophobic transmembrane domain and a cytoplasmic tail of30amino acids.The ligation of B7-H1co-stimulates the growth of human T cell through a receptor differentfrom CD28. Our experiment is to study the influence between radiation and B7-H1positivecells immune escape ability, in order to accumulate useful information in the future targetingtumor cells of radiation and immune therapy. This study plans to observe the effects of radiationon mice GL261cell lines in vitro (including the cell surface B7-H1molecular expression, theability to kill T cells).We are doing a pilot study on the effects of radiation for tumor cells. Thestudy found that GL261cell lines in vitro almost don’t express B7-H1molecular (expressionrate is less than0.1%), and after5and10GY respectively gamma radiation exposure, and at12,24and48hours later, compared with the control, B7-H1expression rate were5.8%,11.2%,11.6%and18.4%,4.3%and3.2%, there is an obvious increase before irradiation. And in acertain period, with the extension of time, the expression rate increases. We suppose thatbecause the cells which do not express B7-H1are massive death. Later B7-H1expression fallsagain without the radiation. We use the method of magnetic beads to sorting out B7-H1positivecells, which used to cocultivation with CTL, and at the same time, GL261cell lines is as thecontrast, after the experiment, we found that sensitization T cells could damage the B7-H1negative control cells more easy.(P=0.006).Comprehensive the study, we found that the radiation have an important effect on theexpression rate of B7-H1in tumor cells, and B7-H1plays an positive role in tumor in theimmune escape of glioblastoma cells.