Gilbert K M, Dresser D W
National Institute for Medical Research, London, United Kingdom.
J Immunol. 1988 Jan 1;140(1):15-20.
Anti-Igh-1b antiserum induced allotype-specific suppression of adult mouse spleen cells in an adoptive transfer system. Suppression of Igh-1b anti-sheep red blood cell plaque-forming cells was measured as late as 4 wk after the injection of allotype heterozygous (Igha/b) spleen cells, antiserum, and sheep red blood cells. Suppression was maintained on retransfer of the allotype-suppressed spleen cells to further irradiated recipients in the absence of additional exogenous anti-allotype antibody. Mixing experiments were performed to test the putative inhibitory effects of allotype-suppressed spleen cells from the first adoptive transfer (stage I) on the antibody response of normal spleen cells in a second adoptive transfer (stage II). No suppression was observed by using unfractionated stage I spleen cells. In contrast, when these allotype-suppressed spleen cells were depleted of T cells, they strongly inhibited the antibody production of admixed normal spleen cells in stage II. This inhibitory activity of antibody-induced stage I spleen cells was directed primarily toward the target allotype, but some suppression of the Igh-1a plaque-forming cell response and total IgG production also occurred. Although removal of adherent cells did not affect the inhibitory activity of allotype-suppressed spleen cells from stage I, removal of Ig+ cells completely abrogated the inhibitory activity. These results suggest that antibody-induced regulatory B cells may play a role in maintaining long term allotype suppression.
在过继转移系统中，抗Igh-1b抗血清可诱导成年小鼠脾细胞产生同种异型特异性抑制。在注射同种异型杂合（Igha/b）脾细胞、抗血清和绵羊红细胞4周后，才检测到Igh-1b抗绵羊红细胞空斑形成细胞的抑制情况。在没有额外外源性抗同种异型抗体的情况下，将同种异型抑制的脾细胞再次转移到进一步照射的受体中时，抑制作用得以维持。进行混合实验以测试第一次过继转移（阶段I）中同种异型抑制的脾细胞对第二次过继转移（阶段II）中正常脾细胞抗体反应的假定抑制作用。使用未分离的阶段I脾细胞未观察到抑制作用。相反，当这些同种异型抑制的脾细胞去除T细胞后，它们在阶段II中强烈抑制混合的正常脾细胞的抗体产生。抗体诱导的阶段I脾细胞的这种抑制活性主要针对靶同种异型，但也发生了对Igh-1a空斑形成细胞反应和总IgG产生的一些抑制。虽然去除贴壁细胞不影响阶段I中同种异型抑制的脾细胞的抑制活性，但去除Ig+细胞完全消除了抑制活性。这些结果表明，抗体诱导的调节性B细胞可能在维持长期同种异型抑制中起作用。
