Fontalin L N, Kondratieva T K, Kondratieva I A, Sidorova E V, Megrabyan T B
Folia Biol (Praha). 1985;31(5):321-32.
The polyclonal immune response was induced in untreated mice and mice treated with cyclophosphamide by the administration of lipopolysaccharide from E. coli or S. marcescens. The number of cells forming antibodies to sheep red blood cells and to trinitrophenyl, and of cells producing immunoglobulins increased. The administration of LPS to mice pretreated with SRBC and CY (tolerant mice) considerably reduced the number of anti-SRBC AFC in comparison with the controls. The tolerogenic treatment did not change the number of anti-TNP AFC and IPC. Analogous results were obtained in genetically athymic (nude) mice and in B mice (thymectomized, lethally irradiated and reconstituted with embryonic liver cells). The results suggest that a deletion or a temporary inactivation of a fraction of the antigen-specific B cells occurs in tolerant mice. This inactivation cannot be explained by the absence of expression of surface immunoglobulins on B cells nor by the activity of suppressor T cells.
通过给予来自大肠杆菌或粘质沙雷氏菌的脂多糖,在未处理的小鼠和用环磷酰胺处理的小鼠中诱导多克隆免疫反应。形成针对绵羊红细胞和三硝基苯基的抗体的细胞数量以及产生免疫球蛋白的细胞数量增加。与对照组相比,向用绵羊红细胞和环磷酰胺预处理的小鼠(耐受小鼠)施用脂多糖显著减少了抗绵羊红细胞抗体形成细胞的数量。致耐受性处理并未改变抗三硝基苯基抗体形成细胞和免疫球蛋白产生细胞的数量。在基因无胸腺(裸)小鼠和B小鼠(胸腺切除、致死性照射并用胚胎肝细胞重建)中获得了类似的结果。结果表明,在耐受小鼠中发生了一部分抗原特异性B细胞的缺失或暂时失活。这种失活不能用B细胞表面免疫球蛋白表达的缺失或抑制性T细胞的活性来解释。