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异基因骨髓移植(Allogeneic Bone Marrow Transplantation,ABMT)后,受体的免疫功能长期缺损,是患者术后极易感染死亡的重要原因之一.本文对ABMT小鼠(C57BL/6→BALB/c)免疫功能缺损的机制进行了探讨,发现ABMT小鼠IL-2产生明显受损;其脾细胞与(C57BL/6小鼠脾细胞一起过继转移到致死量照射的BALB/C小鼠体内,能抑制移植物抗宿主病(GVHD)的发生.去除其脾T细胞后,这种抑制作用丧失,ABMT小鼠脾细胞上清中发现一种非特异的抑制因子,能抑制正常小鼠脾细胞产生混合淋巴细胞反应的能力;能抑制正常小鼠的脾细胞产生IL-2;抑制正常小鼠脾细胞毒T淋巴细胞(CTL)的杀伤活性.用抗Thy-1.2单抗和补体去除ABMT小鼠脾T细胞后,其脾细胞培养上(?)的上述抑制活性丧失.这说明ABMT小鼠脾T(?)细胞活性增强是其免疫功能缺损的重要原因之一,它通过释放非特异的抑制因子执行其免疫抑制功能.
After allogeneic Bone Marrow Transplantation (ABMT), the long-term immunologic impairment of the recipient is one of the most important causes of death in patients with ABMT infection (C57BL / 6 → BALB / c) We found that IL-2 production in ABMT mice was significantly impaired. The splenocytes were inhibited by adoptive transfer of splenocytes (C57BL / 6 mice splenocytes to lethally irradiated BALB / C mice) Graft-versus-host disease (GVHD). After the splenic T cells were removed, this inhibition was abolished. A non-specific inhibitor was found in the spleen cell supernatant of ABMT mice, which inhibited the splenocytes from being mixed in normal mice Lymphocyte reaction; can inhibit the normal mouse spleen cells produce IL-2; inhibit the normal mouse spleen cytotoxic T lymphocytes (CTL) cytotoxic activity with anti-Thy-1.2 monoclonal antibody and complement to remove ABMT mouse spleen T cells, the spleen cell culture (?) On the inhibition of the above activity loss .This shows that ABMT mouse spleen T (?) Cell activity is one of the important reasons for its immune deficiency, which by releasing nonspecific inhibitors Perform its immunosuppressive function.