Phillips R, Lomnitzer R, Rabson A R
Medical Research Council Human Cellular Immunology Unit, School of Pathology, South African Institute for Medical Research, Johannesburg.
J Clin Lab Immunol. 1988 Mar;25(3):139-42.
The proliferative response of NZB/W F1 hybrid mice when activated by sodium periodate (NaIO4) was found to be markedly defective as compared to the response in control NZW mice. This defect was observed in both 4 month old female mice and in 8-10 month old male mice. To determine whether the defect was an intrinsic T cell defect or an accessory cell defect, splenic dendritic cells (DC) were purified and their ability to activate enriched T cells after NaIO4 stimulation was assessed. In mixing experiments it was observed that normal NZW dendritic cells could restore the response of NZB/W F1 hybrid T cells whereas addition of NZB/W F1 dendritic cells to NZW T cells resulted in defective 3H-thymidine incorporation after NaIO4 stimulation. These results indicate that accessory DC of NZB/W F1 mice are defective and unable to support T cell responses to the mitogen NaIO4.
与对照NZW小鼠的反应相比,发现高碘酸钠(NaIO4)激活时NZB/W F1杂交小鼠的增殖反应明显存在缺陷。在4月龄雌性小鼠和8 - 10月龄雄性小鼠中均观察到这种缺陷。为了确定该缺陷是内在的T细胞缺陷还是辅助细胞缺陷,纯化了脾树突状细胞(DC),并评估了其在NaIO4刺激后激活富集T细胞的能力。在混合实验中观察到,正常NZW树突状细胞可以恢复NZB/W F1杂交T细胞的反应,而在NZW T细胞中添加NZB/W F1树突状细胞会导致NaIO4刺激后3H - 胸腺嘧啶核苷掺入缺陷。这些结果表明,NZB/W F1小鼠的辅助性DC存在缺陷,无法支持T细胞对丝裂原NaIO4的反应。