Regulation of the Anti‐Trinitrophenyl Response by Anti‐Idiotype Antibodies a
Regulation of the Anti‐Trinitrophenyl Response by Anti‐Idiotype Antibodies a
复制标题
抗独特型抗体对抗三硝基苯基反应的调节
DOI：
--
复制
发表时间：
1983
影响因子：
5.2
通讯作者：
E. Goidl
中科院分区：
文献类型：
--
作者：
G. Siskind;B. Bhogal;J. Gibbons;M. Weksler;G. Thorbecke;E. Goidl
Jerne' 认为，免疫系统是自我调节的，是独特型 (ids) 和抗独特型 (anti-id) 之间相互作用网络的结果。这一假设的关键预测之一是，在对传统外来抗原的免疫反应过程中，应该会自发产生抗独特型抗体。包括我们自己在内的几个研究小组已经观察到了这种自发产生的自身抗 id。 61o 我们观察到，在某些情况下，测定介质中存在低浓度的半抗原，导致在 Jerne" 测定中观察到的噬斑形成细胞 (PFC) 数量增加，作为检测自身抗独特型的基础。我们建议，自身抗 id 可以结合 Ig附着在潜在抗体分泌细胞的表面，从而引起抗体分泌的可逆抑制。半抗原与抗 id 竞争细胞表面抗原受体 (id)。因此，在存在半抗原的情况下，结合的自身抗id被取代，分泌的抑制被逆转，并且观察到PFC数量的增加。因此，半抗原可增强的 PFC 代表 B 细胞，其 由于自身抗-id与细胞表面独特型的结合，抗体的分泌被阻断。证明使用该测定方法的证据之前已发表6*"，包括（a）能够用半抗原洗脱脾细胞中的一种因子，该因子可以对斑块形成产生特异性半抗原可逆抑制，并且具有与其作为 IgG 一致的结合和抗原特性 自动反ID； (b)事实上，在某些实验条件下，在脾脏中检测到的半抗原可增强的PFC的数量与使用常规酶联免疫吸附测定(ELISA)获得的血清中抗-id的结果相关。通过这种方法，我们证明了在对 T 依赖性和 T 非依赖性抗原的初次和继发反应期间自发产生自身抗 id；'.* 自身抗 id 是由小鼠自发产生的38*'0 兔
It has been suggested by Jerne' that the immune system is self regulated as a consequence of a network of interactions between idiotypes (ids) and anti-idiotypes (anti-id). One of the key predictions from such a hypothesis is that anti-id should be spontaneously produced during the immune response to traditional foreign antigens. Such spontaneous production of auto-anti-id has been observed by several groups2-' including our own.61o We have employed the observation that in some cases the presence of a low concentration of hapten in the assay medium results in an increase in the number of plaque-forming cells (PFC) observed in a Jerne" assay, as the basis for the detection of auto-anti-idiotype We suggested that auto-anti-id can bind to Ig on the surface of potential antibody secreting cells, thereby causing a reversible inhibition of antibody secretion. Hapten competes with anti-id for cell-surface antigen receptors (id). Therefore, in the presence of hapten, bound auto-anti-id is displaced, the inhibition of secretion is reversed, and an increase in the number of PFC is observed. Thus, hapten-augmentable PFC represent B cells whose secretion of antibody has been blocked as a consequence of the binding of auto-anti-id to cell surface idiotype. Evidence justifying the use of this assay has been previously published6*" and includes (a) the ability to elute with hapten a factor from spleen cells that can cause a specific hapten-reversible inhibition of plaque formation and that has binding and antigenic properties consistent with its being an IgG auto-anti-id; (b) the fact that under certain experimental conditions the number of hapten-augmentable PFC detected in the spleen correlates with the results obtained using a conventional enzyme-linked immunosorbent assay (ELISA) for anti-id in the serum. With this approach we have demonstrated that auto-anti-id is produced spontaneously during the primary and secondary responses to both T-dependent and T-independent antigens;'.* auto-anti-id is produced spontaneously by mice38*'0 rabbits