Rose M L, Parrott D M, Bruce R G
Immunology. 1976 Nov;31(5):723-30.
The migration of [125I]UdR-labelled mesenteric lymph node cells in NIH strain mice at various times after inis produced an enhanced accumulation of mesenteric immunoblasts in the small intestine at 2 and 4 days after infection but not at later times. The enhanced migration occurred when using cells from both uninfected and infected donors, denoting an absence of antigenic specificity. This effect is not secondary to a reduced arrival of cells at sites away from the gut in infected mice, but to a primary increase of the arrival in the small intestine. Mesenteric T lymphoblasts (separated on a nylon-wool column) migrated to the small intestine of uninfected recipients and appear to be a major portion of the population which migrate to the gut of infected recipients. Our results were confirmed using 51Cr to label mesenteric cells. We conclude that the parasite causes the small intestine to become more attractive or retentive for mesenteric blast cells early during infection.
在感染[某种寄生虫]后不同时间,对NIH品系小鼠中用[125I]UdR标记的肠系膜淋巴结细胞进行迁移实验,结果显示感染后2天和4天时,小肠中肠系膜免疫母细胞的积累增强,而在之后的时间则没有。当使用未感染和感染供体的细胞时,均出现了增强的迁移现象,这表明不存在抗原特异性。这种效应并非继发于感染小鼠中细胞到达肠道外部位的减少,而是由于到达小肠的细胞数量原发性增加。肠系膜T淋巴母细胞(通过尼龙毛柱分离)迁移至未感染受体的小肠,并且似乎是迁移至感染受体肠道的细胞群体的主要部分。我们使用51Cr标记肠系膜细胞证实了我们的结果。我们得出结论,寄生虫在感染早期会使小肠对肠系膜母细胞更具吸引力或滞留性。