Williams W V, Kyriakos M, Sharp G C, Braley-Mullen H
Department of Medicine, University of Missouri, Columbia 65212.
Cell Immunol. 1987 Oct 15;109(2):397-406. doi: 10.1016/0008-8749(87)90322-4.
Experimental autoimmune thyroiditis (EAT) can be adoptively transferred to normal syngeneic recipients using spleen cells from susceptible strains of mice primed in vivo with mouse thyroglobulin (MTg) and lipopolysaccharide (LPS) following in vitro activation of spleen cells by culture with MTg. Irradiation of recipient animals markedly augments the severity of thyroiditis induced in this system. Irradiation of recipients does not alter the time course of the development of thyroiditis, nor does it alter the requirement for both in vivo priming and in vitro activation of spleen cells for the development of EAT. Spleen cells from EAT-resistant strains of mice (e.g., Balb/c) do not induce EAT in irradiated recipients. Irradiated recipients develop significant levels of anti-MTg antibodies while unirradiated recipients have little detectable antibody response. The augmenting effect of irradiation can be substantially reversed by transferring naive spleen cells to recipients prior to the transfer of MTg/LPS-primed in vitro-activated spleen cells. In addition athymic CBA/Tufts nude mice develop more severe EAT than CBA/Tufts nude/+ littermates following transfer of activated CBA/J spleen cells. These data suggest that natural suppressor cells may regulate the development of EAT at the effector cell level.
实验性自身免疫性甲状腺炎（EAT）可通过将在体外用小鼠甲状腺球蛋白（MTg）培养激活后的、来自用MTg和脂多糖（LPS）在体内致敏的易感小鼠品系的脾细胞，过继转移给正常同基因受体。对受体动物进行照射可显著加重该系统中诱导的甲状腺炎的严重程度。对受体进行照射不会改变甲状腺炎发展的时间进程，也不会改变EAT发展过程中对脾细胞体内致敏和体外激活的需求。来自EAT抗性小鼠品系（如Balb/c）的脾细胞不会在受照射受体中诱导EAT。受照射受体产生显著水平的抗MTg抗体，而未受照射受体几乎没有可检测到的抗体反应。在转移MTg/LPS致敏的体外激活脾细胞之前，将未致敏脾细胞转移给受体，可在很大程度上逆转照射的增强作用。此外，在转移活化的CBA/J脾细胞后，无胸腺的CBA/Tufts裸鼠比CBA/Tufts裸/+同窝小鼠发生更严重的EAT。这些数据表明，天然抑制细胞可能在效应细胞水平调节EAT的发展。
