Binz H, Wigzell H
J Exp Med. 1978 Jan 1;147(1):63-76. doi: 10.1084/jem.147.1.63.
Specific immune unresponsiveness against a given set of histocompatibility antigens can be induced by immunization with autologous, antigen-specific T lymphoblasts. Such unresponsiveness can be transferred by lymphoid cells from autoblast-immunized donors to normal syngeneic recipients. The cells being most efficient in transferring the selective suppression are T lymphocytes from the spleen, especially if of Ly 1-2+3+ phenotype. By using such T lymphocytes we deem it likely that the actual underlying mechanism is one of actual transfer of autoanti-idiotypic killer T cells. In support for this view is the fact that such T cells endowed with exquisite specific, cytolytic reactivity towards autologous idiotype-positive T target cells exist in autoblast immune animals. Significant suppression may also be transferred with T cells of Ly 1+2-3- phenotype or with B cells. Here, we consider the suppressive mechanism to be one of production of autoanti-idiotypic antibodies. By using affinity fraction procedures, it was finally possible to prove that all T-cell suppressive activity resides in a population with true antigen-binding-specific receptors for the relevant idiotypes.
针对特定一组组织相容性抗原的特异性免疫无反应性可通过用自体、抗原特异性T淋巴母细胞进行免疫诱导产生。这种无反应性可通过来自自体母细胞免疫供体的淋巴细胞转移给正常同基因受体。在转移选择性抑制方面最有效的细胞是来自脾脏的T淋巴细胞,特别是Ly 1-2+3+表型的T淋巴细胞。通过使用此类T淋巴细胞,我们认为实际的潜在机制可能是自身抗独特型杀伤性T细胞的实际转移。支持这一观点的事实是,在自体母细胞免疫的动物中存在对自体独特型阳性T靶细胞具有精确特异性细胞溶解反应性的此类T细胞。具有Ly 1+2-3-表型的T细胞或B细胞也可能转移显著的抑制作用。在此,我们认为抑制机制是自身抗独特型抗体产生的机制之一。通过使用亲和分级分离程序,最终有可能证明所有T细胞抑制活性都存在于对相关独特型具有真正抗原结合特异性受体的群体中。