Hayosh N S, Silberg D G, Swanborg R H
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit, MI 48201.
J Neuroimmunol. 1988 Jul;18(4):315-24. doi: 10.1016/0165-5728(88)90052-5.
This paper describes our ongoing investigation of the activation of effector cells of experimental allergic encephalomyelitis (EAE) from nonimmune Lewis rats by sequential culture of spleen cells (SpC) with myelin basic protein (BP) and transfer to syngeneic recipients. We show that SpC initiate the effector cell activation process, whereas thymocytes (Thy) are ineffective. Intermediary recipients of BP-cultured SpC are 'primed' for EAE, but do not develop the disease; this primed state persists for at least 2 months. No evidence was found that suppressor cells account for the failure of the intermediary recipients to develop EAE. The activation process can be inhibited by including monoclonal anti-Ia antibody in the primary culture, indicating that multiple triggering signals are involved in the activation of autoreactive T cells.
本文描述了我们正在进行的一项研究，通过将脾细胞（SpC）与髓鞘碱性蛋白（BP）进行连续培养，然后转移至同基因受体，来激活非免疫性Lewis大鼠实验性变应性脑脊髓炎（EAE）的效应细胞。我们发现SpC启动了效应细胞的激活过程，而胸腺细胞（Thy）则无效。经BP培养的SpC的中间受体对EAE呈“致敏”状态，但不会发病；这种致敏状态至少持续2个月。未发现有证据表明抑制细胞是中间受体未能发生EAE的原因。在原代培养中加入单克隆抗Ia抗体可抑制激活过程，这表明自身反应性T细胞的激活涉及多个触发信号。
