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1
Increased intracellular cyclic adenosine monophosphate inhibits T lymphocyte-mediated cytolysis by two distinct mechanisms.细胞内环状单磷酸腺苷增加通过两种不同机制抑制T淋巴细胞介导的细胞溶解。
J Exp Med. 1988 Jun 1;167(6):1963-8. doi: 10.1084/jem.167.6.1963.
2
Dissection of lymphocyte function-associated antigen 1-dependent adhesion and signal transduction in human natural killer cells shown by the use of cholera or pertussis toxin.利用霍乱毒素或百日咳毒素揭示人类自然杀伤细胞中淋巴细胞功能相关抗原1依赖性黏附和信号转导的剖析
Eur J Immunol. 1996 May;26(5):967-75. doi: 10.1002/eji.1830260502.
3
Pertussis toxin effects on T lymphocytes are mediated through CD3 and not by pertussis toxin catalyzed modification of a G protein.百日咳毒素对T淋巴细胞的作用是通过CD3介导的，而非百日咳毒素催化的G蛋白修饰。
J Immunol. 1989 Mar 1;142(5):1631-8.
4
Inhibitory effect of cholera toxin on human natural cell-mediated cytotoxicity and its augmentation by interferon.霍乱毒素对人自然细胞介导的细胞毒性的抑制作用及其被干扰素增强的作用。
Int J Cancer. 1981 Jan 15;27(1):29-36. doi: 10.1002/ijc.2910270106.
5
Locus of inhibitory action of cAMP-dependent protein kinase in the antigen receptor-triggered cytotoxic T lymphocyte activation pathway.环磷酸腺苷依赖性蛋白激酶在抗原受体触发的细胞毒性T淋巴细胞激活途径中的抑制作用位点。
J Biol Chem. 1988 Feb 15;263(5):2330-6.
6
Role of cAMP in regulating cytotoxic T lymphocyte adhesion and motility.环磷酸腺苷在调节细胞毒性T淋巴细胞黏附与运动中的作用。
Eur J Immunol. 1993 Apr;23(4):790-5. doi: 10.1002/eji.1830230403.
7
Cholera toxin discriminates between murine T lymphocyte proliferation stimulated by activators of protein kinase C and proliferation stimulated by IL-2. Possible role for intracellular cAMP.霍乱毒素可区分蛋白激酶C激活剂刺激的小鼠T淋巴细胞增殖和白细胞介素-2刺激的增殖。细胞内cAMP的可能作用。
J Immunol. 1988 Nov 15;141(10):3429-37.
8
Bacterial toxins affect early events of T lymphocyte activation.细菌毒素影响T淋巴细胞激活的早期事件。
J Clin Invest. 1989 Jan;83(1):234-42. doi: 10.1172/JCI113865.
9
Facilitative actions of the protein kinase-C effector system on hormonally stimulated adenosine 3',5'-monophosphate production by swine luteal cells.蛋白激酶-C效应系统对猪黄体细胞激素刺激的3',5'-环磷酸腺苷生成的促进作用。
Endocrinology. 1989 Nov;125(5):2414-20. doi: 10.1210/endo-125-5-2414.
10
Cholera toxin inhibits interleukin-2-induced, but enhances pertussis toxin-induced T-cell proliferation: regulation by cyclic nucleotides.霍乱毒素抑制白细胞介素-2诱导的T细胞增殖，但增强百日咳毒素诱导的T细胞增殖：环核苷酸的调节作用
Immunology. 1992 Jan;75(1):103-7.

引用本文的文献

1
Odorants specifically modulate chemotaxis and tissue retention of CD4+ T cells via cyclic adenosine monophosphate induction.气味分子通过环磷酸腺苷的诱导特异性调节CD4+ T细胞的趋化性和组织滞留。
J Leukoc Biol. 2016 Oct;100(4):699-709. doi: 10.1189/jlb.1A0914-425RR. Epub 2016 May 6.
2
Increased intracellular Ca2+ induces Ca2+ influx in human T lymphocytes.细胞内钙离子浓度升高会诱导人类T淋巴细胞中的钙离子内流。
Mol Biol Cell. 1993 Feb;4(2):173-84. doi: 10.1091/mbc.4.2.173.
3
Phospholipase C-gamma 1 association with CD3 structure in T cells.磷脂酶C-γ1与T细胞中CD3结构的关联
J Exp Med. 1992 Jan 1;175(1):285-8. doi: 10.1084/jem.175.1.285.
4
Cholera toxin inhibits interleukin-2-induced, but enhances pertussis toxin-induced T-cell proliferation: regulation by cyclic nucleotides.霍乱毒素抑制白细胞介素-2诱导的T细胞增殖，但增强百日咳毒素诱导的T细胞增殖：环核苷酸的调节作用
Immunology. 1992 Jan;75(1):103-7.

本文引用的文献

1
Alteration of the cytotoxic action of sensitized lymphocytes by cholinergic agents and activators of adenylate cyclase.胆碱能药物和腺苷酸环化酶激活剂对致敏淋巴细胞细胞毒性作用的改变。
Proc Natl Acad Sci U S A. 1972 Oct;69(10):2995-9. doi: 10.1073/pnas.69.10.2995.
2
The role of cyclic 3',5' adenosine monophosphate in the specific cytolytic activity of lymphocytes.环磷酸腺苷在淋巴细胞特异性溶细胞活性中的作用。
J Immunol. 1972 Jun;108(6):1526-34.
3
CTL adhesion and antigen recognition are discrete steps in the human CTL-target cell interaction.细胞毒性T淋巴细胞（CTL）的黏附和抗原识别是人类CTL与靶细胞相互作用中的不同步骤。
J Immunol. 1987 Mar 1;138(5):1325-30.
4
The lymphocyte function-associated antigen (LFA)-1 and CD2/LFA-3 pathways of antigen-independent human T cell adhesion.人T细胞非抗原依赖性黏附的淋巴细胞功能相关抗原（LFA）-1和CD2/LFA-3途径。
J Immunol. 1987 Aug 15;139(4):1037-45.
5
T cell receptor tyrosine phosphorylation. Variable coupling for different activating ligands.
J Biol Chem. 1987 Sep 15;262(26):12654-9.
6
Crosslinking of surface antigens causes mobilization of intracellular ionized calcium in T lymphocytes.表面抗原的交联导致T淋巴细胞内游离钙的动员。
Proc Natl Acad Sci U S A. 1987 Mar;84(5):1384-8. doi: 10.1073/pnas.84.5.1384.
7
Regulation of transmembrane signaling by receptor phosphorylation.受体磷酸化对跨膜信号传导的调控。
Cell. 1987 Mar 27;48(6):913-22. doi: 10.1016/0092-8674(87)90700-8.
8
Cholera toxin inhibits the T-cell antigen receptor-mediated increases in inositol trisphosphate and cytoplasmic free calcium.霍乱毒素可抑制T细胞抗原受体介导的肌醇三磷酸和细胞质游离钙的增加。
Proc Natl Acad Sci U S A. 1986 Aug;83(15):5673-7. doi: 10.1073/pnas.83.15.5673.
9
The ability of cytotoxic T cells to recognize HLA-A2.1 or HLA-B7 antigens expressed on murine cells correlates with their epitope specificity.细胞毒性T细胞识别在鼠细胞上表达的HLA - A2.1或HLA - B7抗原的能力与其表位特异性相关。
J Immunol. 1987 Dec 1;139(11):3614-21.
10
The role of K+ in the regulation of the increase in intracellular Ca2+ mediated by the T lymphocyte antigen receptor.钾离子在调节由T淋巴细胞抗原受体介导的细胞内钙离子增加中的作用。
Cell. 1987 Jul 3;50(1):119-27. doi: 10.1016/0092-8674(87)90668-4.

细胞内环状单磷酸腺苷增加通过两种不同机制抑制T淋巴细胞介导的细胞溶解。

Increased intracellular cyclic adenosine monophosphate inhibits T lymphocyte-mediated cytolysis by two distinct mechanisms.

作者信息

Gray L S, Gnarra J, Hewlett E L, Engelhard V H

机构信息

Department of Pathology, University of Virginia School of Medicine, Charlottesville 22908.

出版信息

J Exp Med. 1988 Jun 1;167(6):1963-8. doi: 10.1084/jem.167.6.1963.

DOI:10.1084/jem.167.6.1963
PMID:2838563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2189687/
Abstract

Cholera toxin (CT), but not pertussis toxin (PT), treatment of cloned murine CTL inhibited target cell lysis in a dose-dependent fashion. The effects of CT were mimicked by forskolin and cyclic adenosine monophosphate (cAMP) analogues. Inhibition of cytotoxicity by CT and cAMP analogs was mediated in part by attenuation of conjugate formation. Additionally, both CT and cAMP analogs blocked the increase in intracellular Ca2+ induced by stimulation of the TCR complex by mAbs. These findings indicate that cAMP inhibits the activity of CTL by two distinct mechanisms and suggests a role for this second messenger in CTL-mediated cytolysis.

摘要

霍乱毒素（CT）而非百日咳毒素（PT）处理克隆的小鼠细胞毒性T淋巴细胞（CTL），会以剂量依赖的方式抑制靶细胞裂解。毛喉素和环磷酸腺苷（cAMP）类似物可模拟CT的作用。CT和cAMP类似物对细胞毒性的抑制部分是通过减弱共轭形成来介导的。此外，CT和cAMP类似物均阻断了单克隆抗体刺激TCR复合物诱导的细胞内Ca2+增加。这些发现表明，cAMP通过两种不同机制抑制CTL的活性，并提示这种第二信使在CTL介导的细胞溶解中发挥作用。