Callard R E, Smith C M
Eur J Immunol. 1981 Mar;11(3):206-12. doi: 10.1002/eji.1830110309.
Specific antibody responses to influenza virus were obtained in vitro from human blood mononuclear cells (PBM). The response was T cell-dependent, as shown by separation of PBM into E rosette-positive (E+) and -negative (E-) populations. The histocompatibility requirements for T-B cells interactions in this response were analyzed by recombining E- and E+ fractions from donors with varying degrees of HLA compatibility. No antibody formation was obtained from any allogeneic combination except for the special case of HLA identical siblings. As these experiments included combinations with shared or identical HLA-DR specificities, it was unlikely that genetic restriction alone could account for the failure of T-B cell collaboration. Evidence that suppression was responsible for the lack of antibody formation was obtained from experiments in which allogeneic E+ cells profoundly depressed specific antibody responses of intact PBM. In contrast, no such suppression was seen in pokeweed mitogen-driven polyclonal Ig synthesis for which there are no major histocompatibility complex requirements for T cell help. The suppressor activity of allogeneic E+ cells was found to be radiation-sensitive. By irradiating E+ cells, it was, therefore, possible to test for T cell help across an HLA barrier without unwanted suppressor effects. Under these conditions, (irradiated) E+ cells were able to collaborate with allogeneic E- cells even with no HLA alleles in common. This was true even when autologous monocytes were depleted from the helper E+ population. Supernatants collected from antigen-driven cultures of allogeneic E- and E+ cells were able to replace helper T cells in the specific antibody response to influenza virus. The apparent lack of genetic restriction in these responses might, therefore, be explained by the production of a nonrestricted helper factor.
从人血单核细胞（PBM）中在体外获得了对流感病毒的特异性抗体反应。如将PBM分离为E花环阳性（E +）和阴性（E -）群体所示，该反应是T细胞依赖性的。通过将来自具有不同程度HLA相容性的供体的E -和E +组分重组，分析了该反应中T - B细胞相互作用的组织相容性要求。除了HLA相同的同胞这种特殊情况外，任何同种异体组合均未产生抗体形成。由于这些实验包括具有共享或相同HLA - DR特异性的组合，因此不太可能仅遗传限制就能解释T - B细胞协作失败的原因。从实验中获得了证据，即同种异体E +细胞深刻抑制完整PBM的特异性抗体反应是导致缺乏抗体形成的原因。相比之下，在商陆丝裂原驱动的多克隆Ig合成中未观察到这种抑制作用，而该合成对T细胞辅助没有主要组织相容性复合体要求。发现同种异体E +细胞的抑制活性对辐射敏感。因此，通过照射E +细胞，可以测试跨越HLA屏障的T细胞辅助而不会产生不必要的抑制作用。在这些条件下，（照射过的）E +细胞即使没有共同的HLA等位基因也能够与同种异体E -细胞协作。即使从辅助性E +群体中耗尽自体单核细胞，情况也是如此。从同种异体E -和E +细胞的抗原驱动培养物中收集的上清液能够在对流感病毒的特异性抗体反应中替代辅助性T细胞。因此，这些反应中明显缺乏遗传限制可能是由非限制性辅助因子的产生来解释的。
