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1
Interleukin 1 can replace the requirement for I-A-positive cells in the proliferation of antigen-primed T cells.白细胞介素1可替代抗原致敏T细胞增殖过程中对I-A阳性细胞的需求。
Proc Natl Acad Sci U S A. 1982 Aug;79(15):4747-50. doi: 10.1073/pnas.79.15.4747.
2
Antigen-presenting capacity of guinea pig B lymphocytes in T cell proliferative response in vitro.豚鼠B淋巴细胞在体外T细胞增殖反应中的抗原呈递能力。
Immunobiology. 1983 Aug;165(2):161-74. doi: 10.1016/S0171-2985(83)80057-6.
3
IL 2 restores memory B cell activation by antigen-specific T cell clone variants.白细胞介素2可通过抗原特异性T细胞克隆变体恢复记忆B细胞的激活。
J Immunol. 1986 Jan;136(1):39-43.
4
IL-4 synthesis by in vivo primed keyhole limpet hemocyanin-specific CD4+ T cells. I. Influence of antigen concentration and antigen-presenting cell type.体内致敏的钥孔戚血蓝蛋白特异性CD4 + T细胞合成白细胞介素-4。I. 抗原浓度和抗原呈递细胞类型的影响。
J Immunol. 1992 Dec 1;149(11):3468-76.
5
Long-term CD4+ memory T cells from the spleen lack MEL-14, the lymph node homing receptor.来自脾脏的长期CD4+记忆T细胞缺乏淋巴结归巢受体MEL-14。
J Immunol. 1992 Jan 15;148(2):324-31.
6
Low responsiveness of hepatitis B virus-transgenic mice in antibody response to T-cell-dependent antigen: defect in antigen-presenting activity of dendritic cells.乙肝病毒转基因小鼠对T细胞依赖性抗原的抗体反应低反应性:树突状细胞抗原呈递活性缺陷
Immunology. 1993 Mar;78(3):468-75.
7
Keyhole limpet hemocyanin-propagated Peyer's patch T cell clones that help IgA responses.钥孔戚血蓝蛋白增殖的派尔集合淋巴结T细胞克隆,其有助于IgA反应。
J Immunol. 1988 May 15;140(10):3380-8.
8
Role of macrophages as modulators but not as autonomous accessory cells in the proliferative response of immune T cells to soluble antigen.巨噬细胞在免疫T细胞对可溶性抗原的增殖反应中作为调节者而非自主辅助细胞的作用。
Cell Immunol. 1987 Oct 1;109(1):1-11. doi: 10.1016/0008-8749(87)90287-5.
9
Sodium periodate-induced T cell mitogenesis: an analysis of the requirement for Ia and IL 1.高碘酸钠诱导的T细胞有丝分裂:对Ia和白细胞介素1需求的分析
J Immunol. 1985 Aug;135(2):1137-44.
10
Mechanisms of benzo(a)pyrene-induced modulation of antigen presentation.苯并(a)芘诱导抗原呈递调节的机制。
J Pharmacol Exp Ther. 1987 Aug;242(2):399-404.

引用本文的文献

1
Entamoeba histolytica suppresses gamma interferon-induced macrophage class II major histocompatibility complex Ia molecule and I-A beta mRNA expression by a prostaglandin E2-dependent mechanism.溶组织内阿米巴通过一种前列腺素E2依赖机制抑制γ干扰素诱导的巨噬细胞II类主要组织相容性复合体Ia分子和I-Aβ mRNA表达。
Infect Immun. 1995 Mar;63(3):1089-94. doi: 10.1128/iai.63.3.1089-1094.1995.
2
Fever and immunoregulation: hyperthermia, interleukins 1 and 2, and T-cell proliferation.发热与免疫调节:热疗、白细胞介素1和2以及T细胞增殖。
Yale J Biol Med. 1982 Sep-Dec;55(5-6):437-42.
3
Gamma-interferon induction in human lymphoblasts compared with fresh mononuclear leucocytes: earlier synthesis, rapid shut-off and enhancement of yields by metabolic inhibitors.人淋巴母细胞与新鲜单核白细胞中γ干扰素的诱导:早期合成、快速关闭及代谢抑制剂对产量的提高
Immunology. 1984 May;52(1):175-9.
4
The Fab fragment of a directly activating monoclonal antibody that precipitates a disulfide-linked heterodimer from a helper T cell clone blocks activation by either allogeneic Ia or antigen and self-Ia.一种直接激活的单克隆抗体的Fab片段,该片段能从辅助性T细胞克隆中沉淀出二硫键连接的异二聚体,它可阻断同种异体Ia或抗原及自身Ia介导的激活。
J Exp Med. 1984 May 1;159(5):1397-412. doi: 10.1084/jem.159.5.1397.
5
Dissection of the Poly(Glu60Ala30Tyr10) (GAT)-specific T-cell repertoire in H-2Ik mice. II. The use of monoclonal antibodies to study the recognition of Ia antigens by GAT-reactive T-cell clones.H-2Ik小鼠中聚(Glu60Ala30Tyr10)(GAT)特异性T细胞库的剖析。II. 使用单克隆抗体研究GAT反应性T细胞克隆对Ia抗原的识别。
Immunogenetics. 1983;18(6):559-74. doi: 10.1007/BF00345964.
6
Both a monoclonal antibody and antisera specific for determinants unique to individual cloned helper T cell lines can substitute for antigen and antigen-presenting cells in the activation of T cells.针对单个克隆辅助性T细胞系特有的决定簇的单克隆抗体和抗血清,在T细胞激活过程中都可以替代抗原和抗原呈递细胞。
J Exp Med. 1983 Sep 1;158(3):836-56. doi: 10.1084/jem.158.3.836.
7
The poised B cell: lymphokines induce an Ia-increase and antigen-presenting function in B cells.处于准备状态的B细胞:淋巴因子可诱导B细胞Ia增加及抗原呈递功能。
Yale J Biol Med. 1985 Mar-Apr;58(2):145-52.
8
The relationship between epithelial Ia expression and the inflammatory cell infiltrate during experimental oral carcinogenesis.实验性口腔癌发生过程中上皮Ia表达与炎性细胞浸润之间的关系。
Virchows Arch A Pathol Anat Histopathol. 1988;413(6):521-8. doi: 10.1007/BF00750393.
9
Defective antigen presentation in chronically protein-deprived mice.长期蛋白质缺乏小鼠的抗原呈递缺陷。
Immunology. 1988 Apr;63(4):683-9.
10
The expression of Ia-antigen on nasopharyngeal carcinomas xenografted into nude mice.移植于裸鼠的鼻咽癌中Ia抗原的表达。
Arch Otorhinolaryngol. 1985;242(2):209-15. doi: 10.1007/BF00454423.

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A THREE-CELL INTERACTION REQUIRED FOR THE INDUCTION OF THE PRIMARY IMMUNE RESPONSE in vitro.体外诱导初次免疫反应所需的三细胞相互作用。
Proc Natl Acad Sci U S A. 1968 Oct;61(2):542-7. doi: 10.1073/pnas.61.2.542.
2
T-T cell interactions during cytotoxic T lymphocyte (CTL) responses: T cell derived helper factor (Interleukin 2) as a probe to analyze CTL responsiveness and thymic maturation of CTL progenitors.细胞毒性T淋巴细胞(CTL)应答过程中的T-T细胞相互作用:T细胞衍生的辅助因子(白细胞介素2)作为分析CTL反应性和CTL祖细胞胸腺成熟的探针。
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Studies on the purification and structure-functional relationships of murine lymphocyte activating factor (Interleukin 1).小鼠淋巴细胞激活因子(白细胞介素1)的纯化及结构-功能关系研究
Mol Immunol. 1980 May;17(5):571-7. doi: 10.1016/0161-5890(80)90155-8.
4
Role of Ia-positive cells in the production of T cell-replacing factors: blocking of factor production with anti-Ia serum.Ia 阳性细胞在 T 细胞替代因子产生中的作用:用抗 Ia 血清阻断因子产生。
J Immunol. 1980 Sep;125(3):1224-9.
5
Cellular origins of co-stimulator (IL2) and its activity in cytotoxic T lymphocyte responses.共刺激因子(IL2)的细胞起源及其在细胞毒性T淋巴细胞反应中的活性。
J Immunol. 1980 May;124(5):2231-9.
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Nature. 1980 Feb 14;283(5748):664-6. doi: 10.1038/283664a0.
7
Studies on the role of lymphocyte-activating factor (Interleukin 1) in antigen-induced lymph node lymphocyte proliferation.淋巴细胞激活因子(白细胞介素1)在抗原诱导的淋巴结淋巴细胞增殖中的作用研究。
Cell Immunol. 1980 Sep 1;54(2):382-9. doi: 10.1016/0008-8749(80)90218-x.
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Cell-cell interactions in the T cell proliferative response. I. Analysis of the cell types involved and evidence for nonspecific T cell recruitment.T细胞增殖反应中的细胞间相互作用。I. 所涉及细胞类型的分析及非特异性T细胞募集的证据。
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9
Activation of T lymphocytes by lectins and carbohydrate-oxidizing reagents viewed as an immunological recognition of cell-surface modifications seen in the context of "self" major histocompatibility complex antigens.凝集素和碳水化合物氧化试剂对T淋巴细胞的激活,被视为在“自身”主要组织相容性复合体抗原背景下所见到的细胞表面修饰的一种免疫识别。
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How T lymphocytes recognize antigen.T淋巴细胞如何识别抗原。
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白细胞介素1可替代抗原致敏T细胞增殖过程中对I-A阳性细胞的需求。

Interleukin 1 can replace the requirement for I-A-positive cells in the proliferation of antigen-primed T cells.

作者信息

Durum S K, Gershon R K

出版信息

Proc Natl Acad Sci U S A. 1982 Aug;79(15):4747-50. doi: 10.1073/pnas.79.15.4747.

DOI:10.1073/pnas.79.15.4747
PMID:6981816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC346754/
Abstract

Antigen-primed T cells have been shown to require I-region-compatible adherent cells, as well as the priming antigen, to proliferate in vitro. We postulated that the Ia-recognition event is required for the T cell to induce secretion of the monokine interleukin 1 (IL 1) from adherent cells; the conventionally held view is that Ia is directly required for T cell activation. Our hypothesis predicts that IL I could replace the requirement for Ia+ cells in T cell proliferation assays in vitro. To test this prediction, we depleted keyhole limpet hemocyanin (KLH)-primed C57BL/6 mouse lymph node cells of I-A+ cells by treating with monoclonal anti-I-Ab and complement. As expected, this treatment eliminated the ability of KLH to provoke a proliferative response by primed T cells. Proliferation was restored by providing exogenous IL 1, but only in conjunction with added KLH. The proliferative response of primed T cells could also be blocked by adding anti-I-Ab to culture, and this inhibition could similarly be reversed by providing IL 1 in the presence of the specific antigen KLH. On the basis of these findings we propose a model of T cell activation and discuss its implications.

摘要

抗原致敏的T细胞已被证明在体外增殖时需要I区相容的黏附细胞以及致敏抗原。我们推测,T细胞诱导黏附细胞分泌单核因子白细胞介素1(IL-1)需要Ia识别事件;传统观点认为,T细胞激活直接需要Ia。我们的假设预测,在体外T细胞增殖试验中,IL-1可以取代对Ia⁺细胞的需求。为了验证这一预测,我们用单克隆抗I-Ab和补体处理了血蓝蛋白(KLH)致敏的C57BL/6小鼠淋巴结细胞,以去除其中的I-A⁺细胞。正如预期的那样,这种处理消除了KLH激发致敏T细胞增殖反应的能力。通过提供外源性IL-1可恢复增殖,但前提是同时添加KLH。向培养物中添加抗I-Ab也可阻断致敏T细胞的增殖反应,在存在特异性抗原KLH的情况下提供IL-1同样可逆转这种抑制作用。基于这些发现,我们提出了一个T细胞激活模型并讨论了其意义。