Arai S, Kasho T, Tomita Y, Munakata T, Inoue H, Miyazaki T
Department of Microbiology, Kurume University School of Medicine, Fukuoka.
Microbiol Immunol. 1989;33(11):957-67. doi: 10.1111/j.1348-0421.1989.tb00983.x.
The suppressive effects of mouse recombinant interferon-beta (IFN-beta) on B cell differentiation of MRL/Mp-lpr/lpr (MRL/1) mouse, a model of autoimmune diseases, and C3H/H2 mice, a normal situation, were investigated. Spleen mononuclear cells were cultured in the presence of lipopolysaccharide (LPS), and the suppressive effect of IFN-beta was examined on differentiation of B cells to plaque-forming cells (PFCs) by highly sensitive reversed hemolytic plaque assay. IFN-beta (5,000-10,000 units/ml) suppressed more than 50% of PFCs of both MRL/1 and C3H/H2 mice. This suppressive activity as well as the cytotoxicity of natural killer (NK) cells enhanced by IFN-beta was abrogated by treatment of the spleen cells with anti-asialo GM1 antibody in the presence of complement. This suppressive activity was also abrogated by intravenous administration of 20 microliter/mouse of anti-asialo GM1 12 hr before cultivation of spleen cells. These results suggest that NK cells activated by IFN might be responsible for the immunoregulation in autoimmune diseases.
研究了小鼠重组干扰素-β（IFN-β）对自身免疫性疾病模型MRL/Mp-lpr/lpr（MRL/1）小鼠和正常情况的C3H/H2小鼠B细胞分化的抑制作用。在脂多糖（LPS）存在的情况下培养脾单核细胞，并通过高灵敏度反向溶血空斑试验检测IFN-β对B细胞分化为噬斑形成细胞（PFC）的抑制作用。IFN-β（5000 - 10000单位/毫升）抑制了MRL/1和C3H/H2小鼠超过50%的PFC。在补体存在的情况下，用抗唾液酸GM1抗体处理脾细胞可消除这种抑制活性以及IFN-β增强的自然杀伤（NK）细胞的细胞毒性。在培养脾细胞前12小时，每只小鼠静脉注射20微升抗唾液酸GM1也可消除这种抑制活性。这些结果表明，IFN激活的NK细胞可能在自身免疫性疾病的免疫调节中起作用。
