Urban J F, Noben-Trauth N, Donaldson D D, Madden K B, Morris S C, Collins M, Finkelman F D
United States Department of Agriculture, Beltsville, Maryland 20705, USA.
Immunity. 1998 Feb;8(2):255-64. doi: 10.1016/s1074-7613(00)80477-x.
Although IL-4 induces expulsion of the gastrointestinal nematode parasite, Nippostrongylus brasiliensis, from immunodeficient mice, this parasite is expelled normally by IL-4-deficient mice. This apparent paradox is explained by observations that IL-4 receptor alpha chain (IL-4Ralpha)-deficient mice and Stat6-deficient mice fail to expel N. brasiliensis, and a specific antagonist for IL-13, another activator of Stat6 through IL-4Ralpha, prevents worm expulsion. Thus, N. brasiliensis expulsion requires signaling via IL-4Ralpha and Stat6, and IL-13 may be more important than IL-4 as an inducer of the Stat6 signaling that leads to worm expulsion. Additional observations made in the course of these experiments demonstrate that Stat6 signaling is not required for IL-4 enhancement of IgG1 production and actually inhibits IL-4-induction of mucosal mastocytosis.
尽管白细胞介素-4（IL-4）能促使免疫缺陷小鼠排出胃肠道线虫寄生虫巴西日圆线虫，但IL-4缺陷小鼠却能正常排出这种寄生虫。这一明显的矛盾可通过以下观察结果来解释：缺乏IL-4受体α链（IL-4Rα）的小鼠和缺乏信号转导及转录激活因子6（Stat6）的小鼠无法排出巴西日圆线虫，并且IL-13（另一种通过IL-4Rα激活Stat6的因子）的特异性拮抗剂会阻止蠕虫排出。因此，排出巴西日圆线虫需要通过IL-4Rα和Stat6进行信号传导，并且作为导致蠕虫排出的Stat6信号诱导剂，IL-13可能比IL-4更重要。在这些实验过程中所做的其他观察表明，Stat6信号传导对于IL-4增强IgG1的产生并非必需，实际上还会抑制IL-4诱导的黏膜肥大细胞增多症。
