Yoshida T, Cohen S
Fed Proc. 1982 Jun;41(8):2480-3.
Lymphokine-dependent reactions are subject to various kinds of biological control. These are most readily studied under conditions in which such reactions are suppressed by systemic administration of a relatively large dose of antigen. This effect is known as desensitization of delayed-type hypersensitivity and mimics the state of clinical anergy seen in various granulomatous and lymphoproliferative diseases. Experiments on this type of immune unresponsiveness have revealed that the suppression is due to several lymphokine-dependent mechanisms. Thus, a large amount of circulating lymphokines generated and released at the initial stage of desensitization may be responsible for the general suppression of hypersensitivity reactions through both the loss of mediator gradients from one tissue to another and the preemption of effector cells. In a subsequent step, monocytes and/or macrophages activated by these lymphokines release arachidonic acid metabolites including prostaglandin (PG) E1 and PGE2, which inhibit both the production and the activities of lymphokines. Lymphokines are also suggested as being capable of directly inducing suppressor cells for lymphokine production, thus exerting a feedback inhibition. These lymphokine-dependent multiple suppression mechanisms are important for regulatory processes in cell-mediated immunity.
淋巴细胞因子依赖性反应受到多种生物控制。在通过全身给予相对大剂量抗原抑制此类反应的条件下，这些控制作用最容易得到研究。这种效应被称为迟发型超敏反应的脱敏，它模拟了在各种肉芽肿性疾病和淋巴增殖性疾病中所见的临床无反应状态。对这种类型的免疫无反应性进行的实验表明，抑制作用是由几种淋巴细胞因子依赖性机制引起的。因此，在脱敏初始阶段产生并释放的大量循环淋巴细胞因子，可能通过从一个组织到另一个组织的介质梯度丧失以及效应细胞的抢先占有，导致超敏反应的普遍抑制。在随后的步骤中，被这些淋巴细胞因子激活的单核细胞和/或巨噬细胞释放包括前列腺素（PG）E1和PGE2在内的花生四烯酸代谢产物，这些产物抑制淋巴细胞因子的产生和活性。淋巴细胞因子也被认为能够直接诱导产生淋巴细胞因子的抑制细胞，从而发挥反馈抑制作用。这些淋巴细胞因子依赖性的多重抑制机制对于细胞介导免疫中的调节过程很重要。
