Waldrep J C, Kaplan H J
J Immunol. 1983 Dec;131(6):2746-50.
Injection of trinitrophenyl (TNP)-modified splenocytes (TNP-Sp) into the anterior chamber of the eye results in systemic tolerance to TNP, a phenomenon termed anterior chamber associated immune deviation (TNP-ACAID). Two distinct suppressor pathways develop after the induction of TNP-ACAID. The primary suppressor pathway (I) is antigen-specific, is mediated by a cyclophosphamide (Cy)-sensitive suppressor T cell (Ts-I), and requires a Cy-sensitive auxillary cell. The secondary suppressor pathway (II) is antigen nonspecific, is mediated by a Cy-resistant suppressor T cell (Ts-II), and requires a TNP-pulsed accessory macrophage. Suppression via pathway II is demonstrable only when Ts-I cells are functionally inactivated by Cy. Furthermore, the addition of T cells from Sp containing active Ts-I inhibits Ts-II. This suppression of a suppressor cell (i.e., contrasuppression) is mediated by either Ts-I or a third T cell population, which is also Cy sensitive.
将三硝基苯（TNP）修饰的脾细胞（TNP-Sp）注射到眼前房可导致对TNP的全身耐受，这一现象称为前房相关免疫偏离（TNP-ACAID）。在诱导TNP-ACAID后会形成两种不同的抑制途径。主要抑制途径（I）是抗原特异性的，由环磷酰胺（Cy）敏感的抑制性T细胞（Ts-I）介导，并且需要一个Cy敏感的辅助细胞。次要抑制途径（II）是抗原非特异性的，由Cy抗性的抑制性T细胞（Ts-II）介导，并且需要一个TNP脉冲的辅助巨噬细胞。仅当Ts-I细胞被Cy功能性失活时，通过途径II的抑制才得以证明。此外，来自含有活性Ts-I的脾细胞的T细胞的添加会抑制Ts-II。这种对抑制性细胞的抑制（即反向抑制）由Ts-I或第三种T细胞群体介导，这第三种T细胞群体对Cy也敏感。
