McKenzie G J, Emson C L, Bell S E, Anderson S, Fallon P, Zurawski G, Murray R, Grencis R, McKenzie A N
MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
Immunity. 1998 Sep;9(3):423-32. doi: 10.1016/s1074-7613(00)80625-1.
We report that Th2 cell cultures generated using T cells or splenocytes from IL-13-deficient mice produce significantly reduced levels of IL-4, IL-5, and IL-10 compared with wild-type. In contrast, IL-4 and IL-5 production by mast cells stimulated in vitro with PMA, ionomycin, or IgE cross-linking are unaffected. In vitro Th2 cell differentiation cannot be rescued by the addition of exogenous factors, but in vivo antigen challenge and administration of IL-13 can increase Th2-like cytokine responses as can infection with the parasitic nematode Nippostrongylus brasiliensis. IL-13-deficient mice also have lower basal levels of serum IgE and biased antigen-specific immunoglobulin responses. Thus, IL-13 is an important regulator of Th2 commitment and may therefore play a central role in atopy and infectious diseases.
我们报告称，与野生型相比，使用来自白细胞介素13（IL-13）缺陷小鼠的T细胞或脾细胞生成的辅助性T细胞2（Th2）细胞培养物产生的白细胞介素4（IL-4）、白细胞介素5（IL-5）和白细胞介素10水平显著降低。相比之下，用佛波酯（PMA）、离子霉素或免疫球蛋白E（IgE）交联体外刺激肥大细胞产生IL-4和IL-5不受影响。体外添加外源性因子无法挽救Th2细胞分化，但体内抗原攻击和给予IL-13可增加类似Th2的细胞因子反应，巴西日圆线虫感染也可如此。IL-13缺陷小鼠的血清IgE基础水平也较低，且抗原特异性免疫球蛋白反应存在偏差。因此，IL-13是Th2细胞定向分化的重要调节因子，因此可能在特应性疾病和传染病中起核心作用。
