摘要
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.
In this report we studied the mechanism of the immunodeficiency of the recipients grafted with allogeneic bone marrow. The results indicated that the IL-2 production of ABMT mice was seriously impaired. Further investigation revealed that the spleen cells of ABMT mice were able to suppress GVHD in the lethally irradiated BALB/c mice. After removing the T cells, the spleen cells of ABMT mice lost this inhibitory effect. Furthermore, the supernatant of the spleen cell culture of ABMT mice is able to inhibit the mixed lymphocyte reaction, the IL-2 production and the killing activity of the CTL of normal BALB/c mice. After removal of T cells, the supernatant of the spleen cell culture lost its inhibitory effect. These results suggested that the increased activity of T suppressor secreting a non-specific suppressor factor might be an important mechanism of the immunodeficiency of ABMT mice.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
1990年第3期142-145,共4页
Chinese Journal of Immunology
基金
中国自然科学基金会与加拿大医学研究会合作项目
国家自然科学基金资助
关键词
骨髓移植
异基因
免疫缺损
Allogeneic bone marrow transplantation
T suppressor cell
Immunodeficiency
Graft-versus-host disease
