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首页> 美国卫生研究院文献>Immunology >Coincidence of autoantibody production with the activation of natural killer T cells in α-galactosylceramide-mediated hepatic injury
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Coincidence of autoantibody production with the activation of natural killer T cells in α-galactosylceramide-mediated hepatic injury

机译：在α-半乳糖基神经酰胺介导的肝损伤中自身抗体产生与自然杀伤性T细胞活化的同时发生

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摘要

Natural killer T (NKT) cells are known to be specifically activated by α-galactosylceramide (α-GalCer) via their interaction with CD1d. At that time, NKT cells mediate autoreactivity and eventually induce hepatic injury. As these immune responses resemble acute autoimmune hepatitis, it was examined whether autoantibody production and the activation of autoantibody-producing B-1 cells were accompanied by this phenomenon. Autoantibodies against Hep-2 cells and double-stranded DNA were detected in sera as early as day 3 (showing a peak at day 14) when mice were treated with α-GalCer. On day 3, B220low cells appeared in the liver. These B220low cells were CD5− (i.e. B-1b cells) and CD69+ (an activation marker). Primarily, such B220low cells were present in the peritoneal cavity, but the proportion of B220low cells increased with the administration of α-GalCer even at this site. In parallel with the appearance of B220low cells in the liver, hepatic lymphocytes acquired the potential to produce autoantibodies in in vitro cell culture in the presence of lipopolysaccharide. These results suggested that hepatic injury induced by α-GalCer administration resembled acute autoimmune hepatitis and that the major effector lymphocytes were NKT cells with autoreactivity and autoantibody-producing B-1 cells.
机译：已知自然杀伤T（NKT）细胞通过与CD1d的相互作用而被α-半乳糖基神经酰胺（α-GalCer）特异性激活。那时，NKT细胞介导自身反应性并最终诱发肝损伤。由于这些免疫反应类似于急性自身免疫性肝炎，因此检查了这种现象是否伴随着自身抗体的产生和自身抗体产生的B-1细胞的活化。当用α-GalCer治疗小鼠时，最早在第3天（在第14天出现峰值）就在血清中检测到针对Hep-2细胞和双链DNA的自身抗体。在第3天，肝脏中出现B220 low 细胞。这些B220 low 细胞是CD5 -（即B-1b细胞）和CD69 + （激活标记）。最初，这种B220 low 细胞存在于腹膜腔中，但是即使在该部位施用α-GalCer，B220 low 细胞的比例也会增加。在肝脏中出现B220 low 细胞的同时，肝淋巴细胞具有在脂多糖存在下体外细胞培养中产生自身抗体的潜力。这些结果表明，由α-GalCer给药引起的肝损伤类似于急性自身免疫性肝炎，并且主要的效应淋巴细胞是具有自身反应性的NKT细胞和产生自身抗体的B-1细胞。

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