Machida A, Kumazawa Y, Mizunoe K
Immunology. 1977 Aug;33(2):199-207.
The i.p. immunization with chemically modified antigen (dodecanoyl-bovine serum albumin, d-BSA) emulsified in Freund's incomplete adjuvant (FIA) of CBA mice provoked delayed-type hypersensitivity (DTH), but not any detectable formation of antibody to the original antigen (BSA). Furthermore, it was found that immunization with d-BSA could generate T cells capable of inhibiting the antibody response to hapten on BSA, and the immunosuppressive effects of these T cells were presumably not due to direct action on hapten-primed and antibody producing B cells. These results were obtained from the following experiments: (1) anti-hapten antibody response to dinitrophenylated-BSA (DNP-BSA) was inhibited when the mice had been primed previously with d-BSA in FIA. This inhibition was regulated by the specificity of the carrier, since the mice treated with d-BSA did not inhibit the anti-DNP antibody response after the immunization with DNP-heterologous carrier, i.e. DNP-keyhole limpet haemocyanin (DNP-KLH). (2) The passive transfer of spleen cells, which had been obtained from donors primed with d-BSA in FIA, inhibited the primary anti-DNP antibody response of syngeneic mice after immunization with DNP BSA. (3) Injection of d-BSA-primed spleen cells suppressed an adoptive anti-DNP antibody response in mice which had been irradiated and had previously had their immunocompetence reconstituted by the cell transfers with both DNP-primed and BSA-primed spleen cells. This immunosuppressive effect of d-BSA-primed spleen cells did not act on hapten-primed B cells, since d-BSA-primed spleen cells could not suppress the adoptive secondary antibody response reconstituted by DNP-primed cells and bacterial alpha-amylase (BαA)-primed cells. This finding suggests that a T—T cell interaction exists for the suppression of the anti-DNP antibody response to DNP-BSA by d-BSA-primed cells.
用弗氏不完全佐剂（FIA）乳化的化学修饰抗原（十二烷酰 - 牛血清白蛋白，d - BSA）对CBA小鼠进行腹腔免疫，引发了迟发型超敏反应（DTH），但未检测到针对原始抗原（BSA）的抗体形成。此外，发现用d - BSA免疫可产生能够抑制对BSA上半抗原的抗体反应的T细胞，并且这些T细胞的免疫抑制作用可能不是由于直接作用于半抗原致敏和产生抗体的B细胞。这些结果来自以下实验：（1）当小鼠先前用FIA中的d - BSA致敏时，对二硝基苯基化 - BSA（DNP - BSA）的抗半抗原抗体反应受到抑制。这种抑制受载体特异性的调节，因为用d - BSA处理的小鼠在用DNP - 异源载体即DNP - 钥孔血蓝蛋白（DNP - KLH）免疫后不抑制抗DNP抗体反应。（2）从用FIA中的d - BSA致敏的供体获得的脾细胞的被动转移，抑制了用DNP BSA免疫的同基因小鼠的初次抗DNP抗体反应。（3）注射用d - BSA致敏的脾细胞抑制了经照射且先前通过用DNP致敏和BSA致敏的脾细胞进行细胞转移而重建免疫能力的小鼠的过继性抗DNP抗体反应。用d - BSA致敏的脾细胞的这种免疫抑制作用不作用于半抗原致敏的B细胞，因为用d - BSA致敏的脾细胞不能抑制由DNP致敏细胞和细菌α - 淀粉酶（BαA）致敏细胞重建的过继性二次抗体反应。这一发现表明，在用d - BSA致敏的细胞抑制对DNP - BSA的抗DNP抗体反应中存在T - T细胞相互作用。
