Ito K, Karasawa M, Kawano T, Akasaka T, Koseki H, Akutsu Y, Kondo E, Sekiya S, Sekikawa K, Harada M, Yamashita M, Nakayama T, Taniguchi M
CREST (Core Research for Evolutional Science and Technology) Project and Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Japan.
Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):740-4. doi: 10.1073/pnas.97.2.740.
The immunological mechanisms that regulate abortion are largely unknown. Here, we found that a distinct subset of lymphocytes, Valpha14 NKT cells expressing an invariant antigen receptor encoded by Valpha14/Jalpha281 and Vbeta7 segments, accumulated in the decidua during pregnancy and provoked abortion upon stimulation with alpha-galactosylceramide (alpha-GalCer), a specific ligand for Valpha14 NKT cells. The alpha-GalCer-mediated abortion was not observed in Valpha14 NKT-, IFN-gamma-, tumor necrosis factor alpha-, or perforin-knock-out mice and appeared to be due to the degeneration of embryonic trophoblasts mediated by the activated Valpha14 NKT cells whose perforin-dependent killing and production of IFN-gamma and tumor necrosis factor alpha were essential. The possible role of the decidual Valpha14 NKT cells in the pathogenesis of abortion is discussed.
调节流产的免疫机制在很大程度上尚不清楚。在此，我们发现了一类独特的淋巴细胞亚群，即表达由Valpha14/Jalpha281和Vbeta7基因片段编码的恒定抗原受体的Valpha14 NKT细胞，它们在孕期蜕膜中积聚，并在用α-半乳糖神经酰胺（α-GalCer，Valpha14 NKT细胞的特异性配体）刺激后引发流产。在Valpha14 NKT细胞、干扰素-γ、肿瘤坏死因子α或穿孔素基因敲除小鼠中未观察到α-GalCer介导的流产，这似乎是由于活化的Valpha14 NKT细胞介导的胚胎滋养层细胞变性所致，而这些细胞依赖穿孔素的杀伤作用以及干扰素-γ和肿瘤坏死因子α的产生至关重要。本文讨论了蜕膜Valpha14 NKT细胞在流产发病机制中的可能作用。
