Qin H Y, Suarez W L, Parfrey N, Power R F, Rabinovitch A
Department of Medicine, University of Alberta, Edmonton, Canada.
Autoimmunity. 1992;12(3):193-9. doi: 10.3109/08916939209148459.
We have previously reported that a single injection of complete Freund's adjuvant (CFA) can prevent diabetes appearance in diabetes-prone (DP) BB rats. In this study, we investigated further the mechanism of CFA-induced protection from diabetes. We found that adoptive transfer of splenic cells from CFA-treated DP rats into young DP rats protected the latter from diabetes development. This suggested that CFA-induced protection from diabetes resulted from activation of regulatory (suppressor) cells. Cell mixing experiments in vitro indicated that CFA activated splenic cells with antigen-nonspecific suppressor activity (suppression of lymphoproliferative responses to lipopolysaccharide and to allogeneic splenic cells). Fractionation of splenic cells on Percoll revealed that the suppressor activity resided in low density cells relatively depleted of T-cells, B-cells, macrophages and NK cells. These results suggest that non-specific (natural) suppressor cells in CFA-treated BB rats may be responsible for suppressing autoimmune responses and preventing insulitis and diabetes development.
我们之前曾报道，单次注射完全弗氏佐剂（CFA）可预防糖尿病易感（DP）BB大鼠出现糖尿病。在本研究中，我们进一步探究了CFA诱导的糖尿病预防机制。我们发现，将经CFA处理的DP大鼠的脾细胞过继转移至年轻的DP大鼠体内，可保护后者不发生糖尿病。这表明CFA诱导的糖尿病预防是由调节（抑制）细胞的激活所致。体外细胞混合实验表明，CFA激活了具有抗原非特异性抑制活性的脾细胞（抑制对脂多糖和同种异体脾细胞的淋巴细胞增殖反应）。在Percoll上对脾细胞进行分级分离显示，抑制活性存在于相对缺乏T细胞、B细胞、巨噬细胞和NK细胞的低密度细胞中。这些结果表明，经CFA处理的BB大鼠中的非特异性（天然）抑制细胞可能负责抑制自身免疫反应并预防胰岛炎和糖尿病的发生。
