Stanton T H, Tubbs C, Clagett J
J Immunol. 1985 Dec;135(6):4021-6.
Splenocytes from the motheaten mouse, after stimulation with alloantigen, lack the ability to utilize exogenous interleukin 1 (IL 1) or interleukin 2 (IL 2), express receptors for IL 2, or produce (IL 2). However, in contrast to other models of autoimmunity and immunodeficiency, after mitogen stimulation, motheaten splenocytes produced as much IL 1 or IL 2 as their normal littermates. In addition, these splenocytes expressed functional IL 2 receptors in the same quantity as normal littermate or wild-type splenocytes. Furthermore, motheaten thymocytes and splenocytes, like their normal littermates, respond synergistically to IL 1 on co-stimulation with mitogen, suggesting expression of an IL 1 receptor. Thus, motheaten mouse splenocytes are unable to utilize an antigen-delivered signal and convert it into cytokine production or IL 2 receptor expression. If the antigen signal is bypassed with mitogen, cytokine production and receptor expression appear normal.
受到同种异体抗原刺激后,动性吞噬细胞小鼠的脾细胞缺乏利用外源性白细胞介素1(IL-1)或白细胞介素2(IL-2)的能力,不表达IL-2受体,也不产生IL-2。然而,与其他自身免疫和免疫缺陷模型不同的是,经有丝分裂原刺激后,动性吞噬细胞小鼠的脾细胞产生的IL-1或IL-2与它们的正常同窝仔一样多。此外,这些脾细胞表达的功能性IL-2受体数量与正常同窝仔或野生型脾细胞相同。此外,动性吞噬细胞小鼠的胸腺细胞和脾细胞与它们的正常同窝仔一样,在有丝分裂原共同刺激下对IL-1产生协同反应,提示存在IL-1受体的表达。因此,动性吞噬细胞小鼠的脾细胞无法利用抗原传递的信号并将其转化为细胞因子产生或IL-2受体表达。如果用有丝分裂原绕过抗原信号,细胞因子产生和受体表达看起来是正常的。