Tumor necrosis factor is involved in the T cell-independent pathway of macrophage activation in scid mice.
Tumor necrosis factor is involved in the T cell-independent pathway of macrophage activation in scid mice.
复制标题
肿瘤坏死因子参与 scid 小鼠巨噬细胞激活的 T 细胞非依赖性途径。
作者：
G. Bancroft;K. Sheehan;Robert D. Schreiber;Emil R. Unanue
我们分析了严重联合免疫缺陷（scid）突变小鼠中IFN-γ的T细胞非依赖性产生。scid小鼠的脾细胞分泌高水平的IFN-γ，以响应热杀死的单核细胞增生李斯特菌（HKLM），但不是T细胞刺激ConA。通过预先去除粘附的巨噬细胞来消除这种反应。IFN-γ在体外分泌之前是TNF的快速产生，并且通过添加中和TNF的mAb来抑制。此外，scid小鼠注射抗肿瘤坏死因子单克隆抗体增加感染的严重程度与活李斯特菌和抑制巨噬细胞活化II类MHC的表达。最后，IFN-γ分泌和II类-MHC表达也被去唾液酸GM 1抗体抑制，去唾液酸GM 1是一种已知会损害宿主NK细胞功能的试剂。这些结果表明，TNF是一个关键的细胞因子的T细胞非依赖性途径的巨噬细胞活化在SCID小鼠。
We analyzed the T cell-independent production of IFN-gamma in the severe combined immunodeficiency (scid) mutant mouse. Spleen cells from scid mice secreted high levels of IFN-gamma in response to heat-killed Listeria monocytogenes (HKLM), but not to the T cell stimulus ConA. This response was ablated by prior removal of adherent macrophages. IFN-gamma secretion in vitro was preceded by the rapid production of TNF and was inhibited by addition of neutralizing mAb to TNF. Moreover, injection of scid mice with anti-TNF mAb increased the severity of infection with live Listeria and inhibited macrophage activation for class II-MHC expression. Finally, IFN-gamma secretion and class II-MHC expression were also inhibited by an antibody to asialoGM1, a reagent known to impair host NK cell function. These results suggest that TNF is a critical cytokine in the T cell-independent pathway of macrophage activation in scid mice.