抗原和受体驱动的调节机制。VIII. 抗独特型二级T抑制细胞与交叉反应性独特型阳性、对氨基苯砷酸致敏的T细胞靶标的相互作用导致对独特型阴性、对氨基苯砷酸特异性T细胞的抑制。
Antigen- and receptor-driven regulatory mechanisms. VIII. Suppression of idiotype-negative, p-azobenzenearsonate-specific T cells results from the interaction of an anti-idiotypic second-order T suppressor cell with a cross-reactive-idiotype-positive, p-azobenzenearsonate-primed T cell target.
作者信息
Sy M S, Nisonoff A, Germain R N, Benacerraf B, Greene M I
出版信息
J Exp Med. 1981 Jun 1;153(6):1415-25. doi: 10.1084/jem.153.6.1415.
Abstract
The suppressor pathway that regulates the T cell response to p-azobenzenearsonate (ABA)-coupled cells has been studied. It has been found that the ability of anti-idiotypic second-order T suppressor cells (Ts2) to inhibit T cell-dependent delayed-type hypersensitivity (DTH) responses depended upon the presence of cross-reactive-idiotype (CRI)-bearing T cells present in ABA-primed mice. This suppressor T cell subset, termed Ts2, so exists with CRI-negative T cells that mediate DTH in vivo. It appears that antigen-activated CRI+ Ts3 require signals from the anti-CRI Ts2 subset to suppress DTH reactions in an idiotype-nonspecific manner. The relevance of these observations to a comprehensive scheme of T and B cell regulation is discussed.
摘要
已对调节T细胞对对氨基苯砷酸（ABA）偶联细胞反应的抑制途径进行了研究。已发现抗独特型二级T抑制细胞（Ts2）抑制T细胞依赖性迟发型超敏反应（DTH）的能力取决于ABA致敏小鼠中存在的携带交叉反应性独特型（CRI）的T细胞。这个被称为Ts2的抑制性T细胞亚群与体内介导DTH的CRI阴性T细胞共存。似乎抗原激活的CRI+ Ts3需要来自抗CRI Ts2亚群的信号，以独特型非特异性方式抑制DTH反应。讨论了这些观察结果与T和B细胞调节综合方案的相关性。
相似文献
1
Antigen- and receptor-driven regulatory mechanisms. VIII. Suppression of idiotype-negative, p-azobenzenearsonate-specific T cells results from the interaction of an anti-idiotypic second-order T suppressor cell with a cross-reactive-idiotype-positive, p-azobenzenearsonate-primed T cell target.抗原和受体驱动的调节机制。VIII. 抗独特型二级T抑制细胞与交叉反应性独特型阳性、对氨基苯砷酸致敏的T细胞靶标的相互作用导致对独特型阴性、对氨基苯砷酸特异性T细胞的抑制。
J Exp Med. 1981 Jun 1;153(6):1415-25. doi: 10.1084/jem.153.6.1415.
2
Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.抗原和受体驱动的调节机制。III. 用抗交叉反应性独特型抗体诱导对偶氮苯砷酸盐的迟发型超敏反应。
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3
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J Exp Med. 1980 May 1;151(5):1183-95. doi: 10.1084/jem.151.5.1183.
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J Exp Med. 1980 Mar 1;151(3):528-41. doi: 10.1084/jem.151.3.528.
5
Antigen- and receptor-driven regulatory mechanisms. V. The failure of idiotype-coupled spleen cells to induce unresponsiveness in animals lacking the appropriate VH genes is caused by the lack of idiotype-matched targets.抗原和受体驱动的调节机制。五、在缺乏适当VH基因的动物中，独特型偶联的脾细胞未能诱导无反应性是由于缺乏独特型匹配的靶细胞。
J Exp Med. 1980 Nov 1;152(5):1226-35. doi: 10.1084/jem.152.5.1226.
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Genetic and biological characterization of a T suppressor cell induced by anti-idiotypic antibody.抗独特型抗体诱导的抑制性T细胞的遗传与生物学特性
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7
Antigen- and receptor-driven regulatory mechanisms. I. Induction of suppressor T cells with anti-idiotypic antibodies.抗原和受体驱动的调节机制。I. 用抗独特型抗体诱导抑制性T细胞。
J Exp Med. 1979 Nov 1;150(5):1216-28. doi: 10.1084/jem.150.5.1216.
8
Mechanisms of regulation of cell-mediated immunity. IV. Azobenzenearsonate-specific suppressor factor(s) bear cross-reactive idiotypic determinants the expression of which is linked to the heavy-chain allotype linkage group of genes.细胞介导免疫的调节机制。IV. 偶氮苯胂酸盐特异性抑制因子带有交叉反应性独特型决定簇，其表达与重链同种异型连锁基因群相关。
J Exp Med. 1979 May 1;149(5):1084-98. doi: 10.1084/jem.149.5.1084.
9
Antigen- and receptor-driven regulatory mechanisms. VII. H-2-restricted anti-idiotypic suppressor factor from efferent suppressor T cells.抗原和受体驱动的调节机制。VII. 来自传出抑制性T细胞的H-2限制性抗独特型抑制因子。
J Exp Med. 1981 Feb 1;153(2):450-63. doi: 10.1084/jem.153.2.450.
10
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Specific cellular stimulation in the primary immune response: experimental test of a quantized model.初次免疫应答中的特异性细胞刺激：量化模型的实验测试
Proc Natl Acad Sci U S A. 1982 Feb;79(3):884-8. doi: 10.1073/pnas.79.3.884.
2
Regulatory idiotypes. T helper cells recognize a shared VH idiotope on phosphorylcholine-specific antibodies.调节性独特型。辅助性T细胞识别磷酸胆碱特异性抗体上的一个共享VH独特型。
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Surv Immunol Res. 1982;1(1):93-108. doi: 10.1007/BF02918246.
7
I-J-restricted interactions in the generation of azobenzenearsonate-specific suppressor T cells.偶氮苯胂酸盐特异性抑制性T细胞产生过程中的I-J限制相互作用。
J Exp Med. 1982 Nov 1;156(5):1325-34. doi: 10.1084/jem.156.5.1325.
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Immunoregulation in senescence: increased inducibility of antigen-specific suppressor T cells and loss of cell sensitivity to immunosuppression in aging mice.衰老过程中的免疫调节：衰老小鼠体内抗原特异性抑制性T细胞的诱导能力增强以及细胞对免疫抑制的敏感性丧失。
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Conversion of immunity to suppression by in vivo administration of I-A subregion-specific antibodies.通过体内给予I-A亚区特异性抗体将免疫转化为抑制。
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10
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本文引用的文献
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A single major pathway of T-lymphocyte interactions in antigen-specific immune suppression.抗原特异性免疫抑制中T淋巴细胞相互作用的单一主要途径。
Scand J Immunol. 1981;13(1):1-10. doi: 10.1111/j.1365-3083.1981.tb00104.x.
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Direct evidence for a two-signal mechanism of cytotoxic T-lymphocyte activation.细胞毒性T淋巴细胞激活双信号机制的直接证据。
Nature. 1980 May 15;285(5761):163-5. doi: 10.1038/285163a0.
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Selective suppression of the major idiotypic component of an antihapten response by soluble T cell-derived factors with idiotypic or anti-idiotypic receptors.利用具有独特型或抗独特型受体的可溶性T细胞衍生因子选择性抑制抗半抗原反应的主要独特型成分。
J Exp Med. 1980 May 1;151(5):1213-31. doi: 10.1084/jem.151.5.1213.
4
Antigen- and receptor-driven regulatory mechanisms. IV. Idiotype-bearing I-J+ suppressor T cell factors induce second-order suppressor T cells which express anti-idiotypic receptors.抗原和受体驱动的调节机制。IV. 携带独特型的I-J+抑制性T细胞因子诱导表达抗独特型受体的二级抑制性T细胞。
J Exp Med. 1980 May 1;151(5):1183-95. doi: 10.1084/jem.151.5.1183.
5
Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.抗原和受体驱动的调节机制。III. 用抗交叉反应性独特型抗体诱导对偶氮苯砷酸盐的迟发型超敏反应。
J Exp Med. 1980 Apr 1;151(4):896-909. doi: 10.1084/jem.151.4.896.
6
Antigen- and receptor-driven regulatory mechanisms. VII. H-2-restricted anti-idiotypic suppressor factor from efferent suppressor T cells.抗原和受体驱动的调节机制。VII. 来自传出抑制性T细胞的H-2限制性抗独特型抑制因子。
J Exp Med. 1981 Feb 1;153(2):450-63. doi: 10.1084/jem.153.2.450.
7
Mechanisms of regulation of cell-mediated immunity. VII. Suppressor T cells induced by suboptimal doses of antigen plus an I-J-specific allogeneic effect.细胞介导免疫的调节机制。VII. 次优剂量抗原加I-J特异性同种异体效应诱导的抑制性T细胞。
J Exp Med. 1981 Feb 1;153(2):437-49. doi: 10.1084/jem.153.2.437.
8
Antigen- and receptor-driven regulatory mechanisms. V. The failure of idiotype-coupled spleen cells to induce unresponsiveness in animals lacking the appropriate VH genes is caused by the lack of idiotype-matched targets.抗原和受体驱动的调节机制。五、在缺乏适当VH基因的动物中，独特型偶联的脾细胞未能诱导无反应性是由于缺乏独特型匹配的靶细胞。
J Exp Med. 1980 Nov 1;152(5):1226-35. doi: 10.1084/jem.152.5.1226.
9
Antigen and receptor-driven regulatory mechanisms. VI. Demonstration of cross-reactive idiotypic determinants on azobenzenearsonate-specific antigen-binding suppressor T cells producing soluble suppressor factor(s).抗原和受体驱动的调节机制。VI. 对偶氮苯胂酸盐特异性抗原结合抑制性T细胞上产生可溶性抑制因子的交叉反应性独特型决定簇的证明。
J Immunol. 1980 Dec;125(6):2374-9.
10
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. V. Role of idiotypes in the suppressor pathway.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞反应。V. 独特型在抑制途径中的作用。
J Exp Med. 1980 Jul 1;152(1):161-9. doi: 10.1084/jem.152.1.161.
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