Greene M I, Bach B A, Benacerraf B
J Exp Med. 1979 May 1;149(5):1069-83. doi: 10.1084/jem.149.5.1069.
Delayed type hypersensitivity to the hapten azobenzenearsonate (ABA) can be induced and suppressed by the administration of hapten-coupled syngeneic spleen cells by the appropriate route. Suppressor T cells stimulated by the intravenous administration of ABA-coupled spleen cells have been shown to produce a discrete subcellular factor(s) which is capable of suppressing delayed type hypersensitivity to azobenzenearsonate in the mouse. Such suppressor factors may be produced by the mechanical disruption of suppressor cells or by placing such suppressor cells in culture for 24 h. The suppressor factor(s) (SF) derived from ABA-specific suppressor cells exhibit biological specificity for the suppression of ABA delayed type hypersensitivity (DTH), but not trinitro-phenyl DTH, as well as the capacity to bind to ABA immunoadsorbents. Passage of suppressor factor(s) over reverse immunoadsorbents utilizing a rabbit anti-mouse F(ab')2 antiserum demonstrated that the antigen-specific T-cell derived SF does not bear conventional immunoglobulin markers. The suppressor factor(s) are not immunoglobulin molecules was further demonstrated by the inability of anti-ABA antibodies to suppress ABA DTH. Gel filtration of ABA suppressor factor(s) showed that the majority of the suppressive activity was present in a fraction with molecular weight ranging between 6.8 x 10(4) and 3.3 x 10(4) daltons. We also analyzed for the presence of determinants encoded by the H-2 major histocompatibility complex (MHC) and found that immunoadsorbents prepared utilizing antisera capable of interacting with gene products of the whole or selected gene regions of H-2 MHC, i.e., B10.D2 anti-B10.A and B10 anti-B10.A immunoadsorbents, retained the suppressive activity of ABA-SF. Elution of such columns with glycine HCl buffers (pH 2.8) permitted recovery of specific suppressive activity. Taken collectively such data supports the notion that suppressor T-cell-derived ABA suppressor factors have antigen-binding specificity as well as determinants controlled by the K end of the H-2 MHC. The distribution of strains capable of making SF has also been analyzed. The relationship of the antigen-binding specificity to VH gene products is discussed in this and the companion paper.
通过适当途径给予偶联半抗原的同基因脾细胞，可诱导和抑制对半抗原偶氮苯砷酸盐（ABA）的迟发型超敏反应。静脉注射ABA偶联的脾细胞所刺激的抑制性T细胞已被证明能产生一种离散的亚细胞因子，该因子能够抑制小鼠对偶氮苯砷酸盐的迟发型超敏反应。这种抑制因子可能通过抑制细胞的机械破坏产生，也可能通过将这种抑制细胞培养24小时产生。源自ABA特异性抑制细胞的抑制因子（SF）对偶氮苯砷酸盐迟发型超敏反应（DTH）的抑制具有生物学特异性，但对三硝基苯DTH无抑制作用，并且具有与ABA免疫吸附剂结合的能力。利用兔抗小鼠F（ab'）2抗血清使抑制因子通过反向免疫吸附剂，结果表明抗原特异性T细胞衍生的SF不带有传统的免疫球蛋白标记。抗ABA抗体不能抑制ABA DTH，进一步证明了抑制因子不是免疫球蛋白分子。ABA抑制因子的凝胶过滤显示，大部分抑制活性存在于分子量在6.8×10⁴至3.3×10⁴道尔顿之间的组分中。我们还分析了H-2主要组织相容性复合体（MHC）编码的决定簇的存在情况，发现利用能够与H-2 MHC的全部或选定基因区域的基因产物相互作用的抗体制备的免疫吸附剂，即B10.D2抗B10.A和B10抗B10.A免疫吸附剂，保留了ABA-SF的抑制活性。用甘氨酸盐酸缓冲液（pH 2.8）洗脱此类柱可回收特异性抑制活性。综合这些数据支持这样一种观点，即抑制性T细胞衍生的ABA抑制因子具有抗原结合特异性以及受H-2 MHC的K端控制的决定簇。还分析了能够产生SF的品系分布情况。本文以及配套论文讨论了抗原结合特异性与VH基因产物的关系。
