Mazel S M, Rudensky A Y, Yurin V L
Laboratory of Immunology, All-Union Research Institute for Genetics and Selection of Industrial Microorganisms, Moscow, USSR.
Eur J Immunol. 1990 Apr;20(4):833-9. doi: 10.1002/eji.1830200418.
Immunoglobulin (Ig)-specific T-B cell interactions were studied in the model of T cell recognition of Ig kappa chain Ig kappa-1b allotype in Ig kappa-1-congenic rats. Using Ig kappa-1b-recognizing major histocompatibility complex (MHC)-restricted T helper clones from August rats we have shown that Ig kappa-1b+ B cells from congenic August.1b rats presented Ig kappa-1b epitope of the processed self-synthesized Ig to T clones. This interaction was found to be a bidirectional regulatory event inducing specific MHC-dependent proliferation of both interacting T cell and B cell as well as Ig(Ig kappa-1b) synthesis. Small Ig kappa-1b+ B cells were capable of inducing T clone proliferation and becoming activated in response to the same T clone. Limiting dilution analysis suggested that every tenth cell in Ig kappa-1b+ B cell population is involved in this interaction. The bystander activation of Ig kappa-1a+ B cells by T clones in the presence of irradiated Ig kappa-1b+ spleen cells, if observed, was less than the level of specific Ig kappa-1b+ B cell proliferation. In contrast to a 20-fold increase of Ig(Ig kappa-1b) levels upon stimulation of Ig kappa-1b+/1a+ B cell population from heterozygous (August x August.1b)F1 rats by T clones, a "nonspecific" increase of Ig(Ig kappa-1a) was not observed. This result demonstrates the requirement for direct T-B contact for B cell activation to occur. The data suggest a great functional potency of T-B interactions mediated by T cell recognition of Ig-derived peptide/MHC class II complexes on the B cell surface. The implication of the data for idiotypic regulation enables us to propose the existence of putative idiopeptidic network T-B cell interactions.
在Igκ-1同基因大鼠中，利用T细胞对Igκ链Igκ-1b同种异型的识别模型，研究了免疫球蛋白（Ig）特异性T-B细胞相互作用。使用来自奥古斯特大鼠的识别Igκ-1b的主要组织相容性复合体（MHC）限制性T辅助细胞克隆，我们发现同基因奥古斯特.1b大鼠的Igκ-1b+B细胞将加工后的自身合成Ig的Igκ-1b表位呈递给T细胞克隆。发现这种相互作用是一种双向调节事件，可诱导相互作用的T细胞和B细胞发生特异性MHC依赖性增殖以及Ig（Igκ-1b）合成。小的Igκ-1b+B细胞能够诱导T细胞克隆增殖，并在对相同T细胞克隆的反应中被激活。有限稀释分析表明，Igκ-1b+B细胞群体中每十个细胞就有一个参与这种相互作用。在存在经辐照的Igκ-1b+脾细胞的情况下，T细胞克隆对Igκ-1a+B细胞的旁观者激活（如果观察到）低于特异性Igκ-1b+B细胞增殖水平。与T细胞克隆刺激杂合子（奥古斯特×奥古斯特.1b）F1大鼠的Igκ-1b+/1a+B细胞群体后Ig（Igκ-1b）水平增加20倍形成对比的是，未观察到Ig（Igκ-1a）的“非特异性”增加。该结果证明了B细胞激活需要T-B直接接触。数据表明，T细胞识别B细胞表面的Ig衍生肽/MHC II类复合物介导的T-B相互作用具有强大的功能效力。这些数据对独特型调节的意义使我们能够提出存在假定的独特型肽网络T-B细胞相互作用。
