Mechanisms of regulation of cell-mediated immunity. III. The characterization of azobenzenearsonate-specific suppressor T-cell-derived-suppressor factors.
Mechanisms of regulation of cell-mediated immunity. III. The characterization of azobenzenearsonate-specific suppressor T-cell-derived-suppressor factors.
复制标题
细胞介导的免疫调节机制。 iii。偶氮烯酸特异性抑制剂T-Cell衍生的抑制因子的表征。
DOI：
10.1084/jem.149.5.1069
复制
发表时间：
1979-05-01
影响因子：
15.3
通讯作者：
Benacerraf, B
中科院分区：
文献类型：
--
作者：
Greene, M I;Bach, B A;Benacerraf, B
通过适当途径给予半抗原偶联的同基因脾细胞，可诱导和抑制半抗原偶氮苯甲酸酯(ABA)所致的迟发性超敏反应。静脉注射ABA偶联的脾细胞刺激的抑制性T细胞产生一种离散的亚细胞因子(S)，该因子能抑制小鼠对偶氮苯磺酸的迟发型超敏反应。这种抑制因子可通过机械破坏抑制细胞或将其置于培养24小时而产生。来自ABA特异性抑制细胞的抑制因子(S)(SF)对ABA迟发型超敏反应(DTH)具有生物学特异性，但不能抑制三硝基苯基DTH，并具有与ABA免疫吸附剂结合的能力。用兔抗鼠F(ab‘)2抗血清将抑制因子(S)通过反向免疫吸附剂，证明抗原特异性T细胞来源的SF不具有常规免疫球蛋白标记。抑制因子(S)不是免疫球蛋白分子，进一步证明了抗ABA抗体不能抑制ABA DTH。ABA抑制因子(S)的凝胶过滤表明，大部分抑制活性存在于分子量在6.8×10(4)到3.3×10(4)道尔顿之间的级分中。我们还分析了H-2主要组织相容性复合体(MHC)决定簇的存在，发现用抗血清制备的免疫吸附材料能够与H-2 MHC全基因或部分基因区域的基因产物相互作用，即B10.D2抗B10.A和B10抗B10.A免疫吸附材料，保留了ABA-SF的抑制活性。用甘氨酸盐酸盐缓冲液(pH 2.8)洗脱这些柱，可以恢复特定的抑制活性。综上所述，这些数据支持抑制性T细胞来源的ABA抑制因子具有抗原结合特异性以及由H-2 MHC的K端控制的决定因素的观点。还分析了产生SF的菌株的分布。本文还讨论了VH基因产物与抗原结合特异性的关系。
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.