Sumida T, Taniguchi M
J Immunol. 1985 Jun;134(6):3675-81.
The cellular mechanisms of the antibody-induced suppression of immune responses were analyzed in the keyhole limpet hemocyanin (KLH) system. Some of the monoclonal anti-KLH antibodies, like KLH-specific suppressor T cell factor (KLH-TsF), were demonstrated to suppress the anti-2,4-dinitrophenyl IgG but not IgM plaque-forming cell responses in a KLH-specific and H-2-restricted manner. The anti-KLH antibodies with suppressive activity reacted with, and in turn, stimulated the suppressor hybridoma (34S-281) with the anti-idiotypic receptor complementary to the idiotypic KLH-TsF of the inducer type. Moreover, because the suppressive activity of the anti-KLH antibody was completely abolished by the treatment of responding spleen cells with anti-Lyt-2 and complement, it was apparent that the suppressive antibody activated suppressor T cell pathways. The isotype or affinity of antibodies is not related to the suppressive activity, because suppressive and nonsuppressive antibodies possess a similar affinity belonging to the same Ig isotypes. It also has been demonstrated that the Fc portion is not the functional site, because the F(ab')2 fragment still has the activity. The antibody specificity is found to be important for determining whether the antibody is suppressive or not. In fact, anti-KLH 26, but not other antibodies without activity, recognizes the particular KLH epitope seen by KLH-TsF, and exclusively interacts with the anti-idiotypic suppressor T cells. Thus, the anti-idiotypic suppressor T cell receives signals both from the suppressive anti-KLH antibody and from KLH-TsF, and transmits the antibody-induced suppressor signals to the effector-suppressor pathway. The size of the repertoire of anti-idiotypic suppressor T cells involved in the suppression seems to be very limited, because only four out of 120 monoclonal anti-KLH antibodies were found to have suppressor activity. The possible mechanisms of the cell interaction mediated by the suppressive antibody are discussed.
在钥孔戚血蓝蛋白（KLH）系统中分析了抗体诱导的免疫反应抑制的细胞机制。一些单克隆抗KLH抗体，如KLH特异性抑制性T细胞因子（KLH-TsF），被证明以KLH特异性和H-2限制性方式抑制抗2,4-二硝基苯基IgG但不抑制IgM空斑形成细胞反应。具有抑制活性的抗KLH抗体与诱导型KLH-TsF的独特型具有互补抗独特型受体的抑制性杂交瘤（34S-281）发生反应，进而刺激该杂交瘤。此外，由于用抗Lyt-2和补体处理反应性脾细胞可完全消除抗KLH抗体的抑制活性，因此很明显抑制性抗体激活了抑制性T细胞途径。抗体的同种型或亲和力与抑制活性无关，因为抑制性和非抑制性抗体具有属于相同Ig同种型的相似亲和力。还已证明Fc部分不是功能位点，因为F(ab')2片段仍具有活性。发现抗体特异性对于确定抗体是否具有抑制性很重要。事实上，抗KLH 26而非其他无活性的抗体识别KLH-TsF所见的特定KLH表位，并仅与抗独特型抑制性T细胞相互作用。因此，抗独特型抑制性T细胞从抑制性抗KLH抗体和KLH-TsF两者接收信号，并将抗体诱导的抑制信号传递至效应抑制途径。参与抑制的抗独特型抑制性T细胞库的大小似乎非常有限，因为在120种单克隆抗KLH抗体中仅发现4种具有抑制活性。讨论了由抑制性抗体介导的细胞相互作用的可能机制。
