Guo L, Hu-Li J, Zhu J, Pannetier C, Watson C, McKenzie G J, McKenzie A N, Paul W E
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Nat Immunol. 2001 May;2(5):461-6. doi: 10.1038/87778.
Interleukin 13-deficient (IL-13-/-) mice express a defect in priming for IL-4 production that is not corrected by adding IL-13 to the priming culture. This is partly accounted for by the consumption of IL-4 without endogenous replacement during culture of IL-13-/- CD4+ T cells. We examined cells from mice in which disrupted Il13 was linked to wild-type Il4 on one chromosome and wild-type Il13 was linked to a "knocked-in" green fluorescent protein (Gfp) gene in the Il4 locus. Our results show that the deficit in IL-4 production was due, at least in part, to a cis effect, in which disrupted Il13 diminished IL-4 production from the linked Il4 gene.
白细胞介素13缺陷（IL-13-/-）小鼠在启动白细胞介素4（IL-4）产生方面存在缺陷，在启动培养物中添加IL-13并不能纠正该缺陷。这部分是由于在IL-13-/- CD4+ T细胞培养过程中IL-4被消耗而没有内源性补充。我们检查了来自这样的小鼠的细胞，在这些小鼠中，一条染色体上破坏的Il13与野生型Il4相连，而野生型Il13与Il4基因座中的“敲入”绿色荧光蛋白（Gfp）基因相连。我们的结果表明，IL-4产生的缺陷至少部分归因于顺式效应，其中破坏的Il13减少了连锁的Il4基因产生的IL-4。
