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对半抗原4-羟基-3-硝基苯乙酰的半抗原特异性T细胞应答。III. 效应性抑制性T细胞的相互作用受H-2和免疫球蛋白重链可变区(Igh-V)基因的限制。

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. III. Interaction of effector suppressor T cells is restricted by H-2 and Igh-V genes.

作者信息

Weinberger J Z, Benacerraf B, Dorf M E

出版信息

J Exp Med. 1980 Jun 1;151(6):1413-23. doi: 10.1084/jem.151.6.1413.

DOI:10.1084/jem.151.6.1413
PMID:6445931
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2185884/
Abstract

4-Hydroxy-3-nitrophenyl acetyl (NP)-derivatized syngeneic spleen cells administered intravenously induced a population of suppressor T cells that could suppress mice previously primed to NP. The effect was demonstrable when the suppressor cells were transferred to NP-primed mice on the day of challenge for delayed-type hypersensitivity (DTH) responses. In contrast to the suppressor T cell population, which abrogates 5-iodo derivative of NP (NIP)-specific DTH responses when administered before antigen priming, the effector-phase suppressors did not efficiently suppress NIP-specific DTH responses, and were not lysed by treatment with antiidiotype plus complement. Adoptive transfer experiments between major histocompatibility complex and allotype congenic strains of mice allowed demonstration of both Igh-V and I-A restrictions in the transfer of this cell population. The implications of these data in terms of network theories and proposed cellular models for negative immunoregulation were discussed.

摘要

静脉注射4-羟基-3-硝基苯乙酰(NP)衍生的同基因脾细胞可诱导出一群抑制性T细胞,这些细胞能够抑制先前已对NP致敏的小鼠。当在迟发型超敏反应(DTH)攻击当天将抑制性细胞转移到已用NP致敏的小鼠体内时,这种效应是可证实的。与在抗原致敏前给予时可消除NP的5-碘衍生物(NIP)特异性DTH反应的抑制性T细胞群体不同,效应期抑制细胞不能有效地抑制NIP特异性DTH反应,并且用抗独特型加补体处理后不会被裂解。在主要组织相容性复合体和小鼠同种异型同基因品系之间进行的过继转移实验表明,在这种细胞群体的转移中存在Igh-V和I-A限制。讨论了这些数据在网络理论和提出的负性免疫调节细胞模型方面的意义。

相似文献

1
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. III. Interaction of effector suppressor T cells is restricted by H-2 and Igh-V genes.对半抗原4-羟基-3-硝基苯乙酰的半抗原特异性T细胞应答。III. 效应性抑制性T细胞的相互作用受H-2和免疫球蛋白重链可变区(Igh-V)基因的限制。
J Exp Med. 1980 Jun 1;151(6):1413-23. doi: 10.1084/jem.151.6.1413.
2
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VI. Evidence for different T cell receptors in cells that mediate H-21-restricted and H-2D-restricted cutaneous sensitivity responses.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。VI. 介导H-2I限制性和H-2D限制性皮肤敏感反应的细胞中不同T细胞受体的证据。
J Exp Med. 1980 Dec 1;152(6):1554-62. doi: 10.1084/jem.152.6.1554.
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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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Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。
J Immunol. 1980 Oct;125(4):1601-5.
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Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VIII. Suppressor cell pathways in cutaneous sensitivity responses.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞反应。VIII. 皮肤敏感性反应中的抑制细胞途径。
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4-Hydroxy-3-nitrophenyl (NP) acetyl-hapten specific lymphocyte proliferation. I. Mice bearing Igh-1b allotype can cross-react with 4-hydroxy-5-iodo-3-nitrophenyl (NIP) acetyl hapten.4-羟基-3-硝基苯基(NP)乙酰半抗原特异性淋巴细胞增殖。I. 携带Igh-1b同种异型的小鼠可与4-羟基-5-碘-3-硝基苯基(NIP)乙酰半抗原发生交叉反应。
Microbiol Immunol. 1984;28(4):471-9. doi: 10.1111/j.1348-0421.1984.tb00698.x.
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Hapten-specific T-cell responses to 4-hydroxy-3-nitrophenyl acetyl. I. Genetic control of delayed-type hypersensitivity by VH and I-A-region genes.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。I. VH和I-A区基因对迟发型超敏反应的遗传控制。
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Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. IX. Characterization of Idiotype-specific effector-phase suppressor cells on plaque-forming cell responses in vitro.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。IX. 体外针对空斑形成细胞应答的独特型特异性效应期抑制细胞的特性
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Anti-receptor antibody-induced suppression of murine H-Y-specific delayed-type hypersensitivity responses.抗受体抗体诱导的小鼠H-Y特异性迟发型超敏反应的抑制
Eur J Immunol. 1981 Aug;11(8):626-31. doi: 10.1002/eji.1830110807.
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Hapten-specific T-cell responses to 4-hydroxy-3-nitrophenyl acetyl. II. Demonstration of idiotypic determinants on suppressor T cells.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。II. 抑制性T细胞上独特型决定簇的证明。
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引用本文的文献

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Special regulatory T-cell review: A rose by any other name: from suppressor T cells to Tregs, approbation to unbridled enthusiasm.特殊调节性T细胞综述:换个名字的玫瑰:从抑制性T细胞到调节性T细胞,从认可到过度热情。
Immunology. 2008 Jan;123(1):20-7. doi: 10.1111/j.1365-2567.2007.02779.x.
2
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VII. Idiotype-specific suppression of plaque-forming cell responses.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。VII. 独特型特异性对空斑形成细胞应答的抑制作用
J Exp Med. 1981 Mar 1;153(3):640-52. doi: 10.1084/jem.153.3.640.
3
Balb/c T cells have the potential to recognize the TEPC 15 prototype antibody and its somatic variants.Balb/c T细胞有识别TEPC 15原型抗体及其体细胞变体的潜力。
J Exp Med. 1981 Oct 1;154(4):1178-87. doi: 10.1084/jem.154.4.1178.
4
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. IX. Characterization of Idiotype-specific effector-phase suppressor cells on plaque-forming cell responses in vitro.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞应答。IX. 体外针对空斑形成细胞应答的独特型特异性效应期抑制细胞的特性
J Exp Med. 1981 Jun 1;153(6):1445-56. doi: 10.1084/jem.153.6.1445.
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Contact sensitivity to azobenzenearsonate and its inhibition after interaction of sensitized cells with antigen-conjugated cells.对偶氮苯胂酸盐的接触敏感性及其在致敏细胞与抗原结合细胞相互作用后的抑制作用。
J Exp Med. 1981 May 1;153(5):1124-37. doi: 10.1084/jem.153.5.1124.
6
Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VIII. Suppressor cell pathways in cutaneous sensitivity responses.对半抗原4-羟基-3-硝基苯乙酰的特异性T细胞反应。VIII. 皮肤敏感性反应中的抑制细胞途径。
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Tolerance for self IG at the level of the Ly1+ T cell.Ly1+ T细胞水平对自身免疫球蛋白的耐受性。
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本文引用的文献

1
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.
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The mechanism of immunological unresponsiveness to picryl chloride and the possible role of antibody mediated depression.对苦味酰氯免疫无反应性的机制及抗体介导抑制的可能作用。
Clin Exp Immunol. 1971 Jul;9(1):111-21.
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Depression of the T cell phenomenon of contact sensitivity by T cells from unresponsive mice.无反应小鼠的T细胞对接触敏感性T细胞现象的抑制作用。
Nature. 1973 Jul 27;244(5413):227-8. doi: 10.1038/244227a0.
4
Towards a network theory of the immune system.迈向免疫系统的网络理论。
Ann Immunol (Paris). 1974 Jan;125C(1-2):373-89.
5
Inheritance of antibody specificity. I. Anti-(4-hydroxy-3-nitrophenyl)acetyl of the mouse primary response.抗体特异性的遗传。I. 小鼠初次免疫应答中的抗(4-羟基-3-硝基苯基)乙酰抗体
J Exp Med. 1974 Dec 1;140(6):1498-510. doi: 10.1084/jem.140.6.1498.
6
Properties of the antigen-specific suppressive T-cell factor in the regulation of antibody response of the mouse. III. Dual gene control of the T-cell-mediated suppression of the antibody response.小鼠抗体应答调节中抗原特异性抑制性T细胞因子的特性。III. T细胞介导的抗体应答抑制的双基因控制。
J Exp Med. 1976 Jul 1;144(1):20-31. doi: 10.1084/jem.144.1.20.
7
Idiotypic analysis of anti-GAT antibodies. I. Presence of common idiotypic specificities in both responder and nonresponder mice.抗GAT抗体的独特型分析。I. 应答和非应答小鼠中共同独特型特异性的存在。
J Immunol. 1978 Sep;121(3):1034-9.
8
A mendelian idiotype is demonstrable in the heteroclitic anti-NP antibodies of the mouse.在小鼠的特异性抗核蛋白抗体中可证实孟德尔个体基因型。
Eur J Immunol. 1978 Feb;8(2):105-11. doi: 10.1002/eji.1830080207.
9
Soluble factors in tolerance and contact sensitivity to 2,4-dinitrofluorobenzene in mice. III. Histocompatibility antigens associated with the hapten dinitrophenol serve as target molecules on 2,4-dinitrofluorobenzene-immune T cells for soluble suppressor factor.小鼠对2,4-二硝基氟苯耐受性和接触敏感性中的可溶性因子。III. 与半抗原二硝基苯酚相关的组织相容性抗原作为2,4-二硝基氟苯免疫T细胞上可溶性抑制因子的靶分子。
J Exp Med. 1979 Dec 1;150(6):1432-47. doi: 10.1084/jem.150.6.1432.
10
Suppressor T-cell mechanisms in contact sensitivity. III. Apparent non-major histocompatibility complex restriction is a result of multiple sets of major histocompatibility complex-specific suppressor T cells induced by syngeneic 2,4-dinitrophenyl-modified lymphoid cells.接触敏感性中的抑制性T细胞机制。III. 明显的非主要组织相容性复合体限制是由同基因2,4-二硝基苯基修饰的淋巴细胞诱导的多组主要组织相容性复合体特异性抑制性T细胞的结果。
J Exp Med. 1979 Sep 19;150(3):676-92. doi: 10.1084/jem.150.3.676.