Yankelevich B, Soldatenkov V A, Hodgson J, Polotsky A J, Creswell K, Mazumder A
Bone Marrow Transplantation Program, Lombardi Cancer Center, Department of Radiation Medicine Georgetown University Medical Center, Washington, DC, 20007, USA.
Cell Immunol. 1996 Mar 15;168(2):229-34. doi: 10.1006/cimm.1996.0070.
We have recently demonstrated that a short-term treatment of parental splenocytes with the B subunit of cholera toxin (CT-B) abrogates the development of acute GVHD in F1 hybrid mice transplanted with these cells. In order to obtain better insight into the mechanism of the action of CT-B, we studied the effect of CT-B on survival of purified murine T cells and their subsets. We show that treatment with B subunit stimulates apoptosis in T cells, detectable following incubation in vitro. Although apoptosis was noticed in both CD8+ and CD4+ T cell subsets, the treatment preferentially stimulates programmed cell death (PCD) in CD8+ population. Thus, immunosuppressive action of CT-B in vivo may be in part due to its ability to eliminate CD8+ T cells.
我们最近证明,用霍乱毒素B亚基(CT-B)对亲代脾细胞进行短期处理,可消除移植了这些细胞的F1杂交小鼠急性移植物抗宿主病(GVHD)的发生。为了更深入了解CT-B的作用机制,我们研究了CT-B对纯化的小鼠T细胞及其亚群存活的影响。我们发现,用B亚基处理可刺激T细胞凋亡,体外孵育后即可检测到。虽然在CD8+和CD4+ T细胞亚群中均观察到凋亡,但该处理优先刺激CD8+群体中的程序性细胞死亡(PCD)。因此,CT-B在体内的免疫抑制作用可能部分归因于其消除CD8+ T细胞的能力。