MODE OF ACTION OF THYMUS DERIVED (T) SUPPRESSOR AND AMPLIFIER CELLS

先前体内CD4+T细胞的耗尽导致显著的 对几种细菌的抗体反应量的降低 多糖类抗原，未知需要CD4+辅助性T细胞 开始产生抗体。这种压制似乎是居中的。 通过残存的CD8+抑制T细胞的抑制作用 (TS)；在没有CD4+放大器T的情况下，它们的影响变得主要 以积极和相反的方式驱动免疫B的细胞(Ta) 细胞对抗原的反应进一步增殖。通过以下方式治疗 各种重组淋巴因子(如IL-2、IL-4、IL-5，但不包括IL-6) 在体内增加了ts活性的表达；因此，ts活性是 受淋巴因子的影响很大，淋巴因子影响活化和/或 T_s的扩展。同样，TS一旦被激活，就会获得一个细胞表面 受体和/或拥有一种生化途径， 对细菌单磷酰基的阻断或灭活敏感 脂蛋白A(MPL)。这种失活似乎仅限于 经相同或更大剂量的药物治疗后TS活性的表达 MPL的量对其他几种基因的表达没有不良影响 检测T细胞功能。

The prior in vivo depletion of CD4+ T cells resulted in a significant decrease in the magnitude of the antibody response to several bacterial polysaccharide antigens, not know to require CD4+ helper T cells to initiate antibody production. Such suppression appears to be mediated by the inhibitory effects exerted by remaining CD8+ suppressor T cells (Ts); their effects become dominant in the absence of CD4+ amplifier T cells (Ta) that act in a positive and opposing manner to drive immune B cells to proliferate further in response to antigen. Treatment with various recombinant lymphokines (e.g., IL-2, IL-4, IL-5, but not IL-6) increased the expression of Ts activity in vivo; thus, Ts activity is effected greatly by lymphokines that influence the activation and/or expansion of Ts. Also, Ts, once activated, acquire a cell surface receptor and/or possess a biochemical pathway that is extremely sensitive to being blocked or inactivated by bacterial monophosphoryl lipid A (MPL). Such inactivation appears to be restricted to the expression of Ts activity since treatment with the same or larger amounts of MPL has no adverse effect on the expression of several other T cell functions examined.