Polak L, Rinck C
J Invest Dermatol. 1978 Feb;70(2):98-104. doi: 10.1111/1523-1747.ep12541235.
Contact sensitivity to dinitrochlorobenzene (DNCB) in guinea pigs could be rapidly suppressed by intravenous injection of dinitrobenzene sulfonic acid sodium salt (DNBSO3). This suppression is transient and antigen-specific. Macrophages from desensitized animals are not inactivated as shown by their ability to react, both in vivo and in vitro to lymphokines produced in a separate system. Therefore, effector lymphocytes are considered the target for the desensitizing antigen. Using an adoptive transfer system it was demonstrated that effector lymphocytes are inactivated by a direct effect of the hapten. Since this inactivation can be reversed by trypsin treatment, a receptor blockade of effector lymphocytes is proposed as the mechanism of desensitization of DNCB-contact sensitive guinea pigs. This does not exclude the possibility that additional mechanisms such as suppressor cells, compartmentalization or endogenous proliferation of lymph node lymphocytes may play an additional role.
豚鼠对二硝基氯苯(DNCB)的接触敏感性可通过静脉注射二硝基苯磺酸钠盐(DNBSO3)迅速受到抑制。这种抑制是短暂的且具有抗原特异性。脱敏动物的巨噬细胞并未失活,这可通过它们在体内和体外对在另一个系统中产生的淋巴因子作出反应的能力得以证明。因此,效应淋巴细胞被认为是脱敏抗原的作用靶点。利用过继转移系统证明,效应淋巴细胞因半抗原的直接作用而失活。由于这种失活可通过胰蛋白酶处理逆转,因此提出效应淋巴细胞的受体阻断是DNCB接触敏感豚鼠脱敏的机制。这并不排除诸如抑制细胞、分隔或淋巴结淋巴细胞的内源性增殖等其他机制可能起额外作用的可能性。