ANTI-IDIOTYPIC CONTROL OF NEURAL AND ALLERGIC DISEASES

C57 B1/6小鼠实验性自身免疫性重症肌无力 通过用电鳐免疫，乙酰胆碱受体已被调节， 通过体内施用抑制性T细胞系而减弱， 来自免疫动物的淋巴结细胞的克隆。 机制 目前正在研究这种抑制与 抗独特型免疫以及 抑制因子 抑制细胞的身份将是 其特征在于其表面标记，包括独特型标记， 含有细胞器的细胞内酶。 它们的体外作用将是 根据致敏细胞对抗原的增殖及其 对抗乙酰胆碱受体二抗产生的影响 体外 在体内注射这些细胞后， EAMG的生物学效应及其对EAMG的影响 分布和归巢的受体动物，他们的生存与一个 而不存在白细胞介素II。 持续时间和特异性 将评估它们在受体动物中的作用，并提供证据， 对抗第二波携带抗独特型抗体的T细胞的发展， 研究的受体。 这些线将通过其表面标记、 “帮助”B细胞在体外和体内产生抗AChR抗体， 在体内产生迟发型超敏反应。 我们将确定 如果疾病可以通过辅助细胞系的细胞转移产生， 是否存在抗原以及AChR免疫是否产生疾病 可以通过预先用减毒细胞系处理来阻断。

Experimental autoimmune myasthenia gravis (EAMG) produced in C57B1/6 mice by immunization with Torpedo acetylcholine receptor has been modulated and attenuated by the in vivo administration of suppressor T cell lines and clones derived from lymph node cells from immunized animals. The mechanism of this suppression is being investigated with respect to its relationship to anti-idiotypic immunity and also with respect to the production of suppressor factors. The identity of the suppressor cells will be characterized by their surface markers, including idiotypic markers and intracellular enzyme containing organelles. Their in vitro action will be determined upon proliferation of sensitized cells to antigen and their effect upon secondary anti-acetylcholine receptor antibody production in vitro. The injection of these cells in vivo will be followed by their biologic influence on the course of development of EAMG as well as their distribution and homing in the recipient animal, their survival with an without the presence of interleukin II. The duration and specificity of their action in the recipient animal will be assessed and evidence for or against the development of a second wave of T cells bearing anti-idiotypic receptors investigated. These lines will be characterized by their surface markers, ability to "help" B cells produce anti-AChR antibody in vitro and in vivo, and to produce delayed type hypersensitivity reactions in vivo. We will determine if disease can be produced by means of cell transfers with helper lines in the absence of antigen and whether disease produced by AChR immunization can be blocked by prior treatment with attenuated cell lines.