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淋巴细胞介导的细胞溶解机制。

Mechanisms of lymphocyte-mediated lysis.

作者信息

Joag S, Zychlinsky A, Young J D

机构信息

Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

出版信息

J Cell Biochem. 1989 Mar;39(3):239-52. doi: 10.1002/jcb.240390304.

DOI:10.1002/jcb.240390304
PMID:2651463
Abstract

Cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells use multiple mechanisms to destroy their target cells. Pore formation resulting in osmotic lysis of the target is one mechanism; the pore-forming protein (perforin) responsible for this activity has been purified. Antigenically and functionally it resembles proteins of the membrane attack complex of complement. The other known mediators of cytotoxicity appear to be closely interrelated. Tumor necrosis factor (TNF), lymphotoxin (LT), and leukalexin are the three members of this group that have been purified, although their mechanisms of action are still unknown. CTLs fragment the DNA of target cells, as do TNF, LT, and leukalexin; this may be one of the mechanisms of action of these mediators. CTLs and NK cells do not self lyse. The basis of this phenomenon is unclear, although recent advances have shed some light on the problem.

摘要

细胞毒性T淋巴细胞(CTLs)和自然杀伤(NK)细胞利用多种机制破坏靶细胞。导致靶细胞渗透性裂解的孔形成是一种机制;负责此活性的孔形成蛋白(穿孔素)已被纯化。在抗原性和功能上,它类似于补体膜攻击复合物的蛋白质。其他已知的细胞毒性介质似乎密切相关。肿瘤坏死因子(TNF)、淋巴毒素(LT)和白细胞毒素是该组中已被纯化的三个成员,尽管它们的作用机制仍不清楚。CTLs会使靶细胞的DNA片段化,TNF、LT和白细胞毒素也会如此;这可能是这些介质的作用机制之一。CTLs和NK细胞不会自我裂解。尽管最近的进展为这个问题提供了一些线索,但这种现象的基础尚不清楚。

相似文献

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Mechanisms of lymphocyte-mediated lysis.淋巴细胞介导的细胞溶解机制。
J Cell Biochem. 1989 Mar;39(3):239-52. doi: 10.1002/jcb.240390304.
2
Cellular mechanisms of lymphocyte-mediated lysis of tumor cells.淋巴细胞介导的肿瘤细胞裂解的细胞机制。
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Structural/functional similarity between proteins involved in complement- and cytotoxic T-lymphocyte-mediated cytolysis.补体和细胞毒性T淋巴细胞介导的细胞溶解相关蛋白之间的结构/功能相似性。
Nature. 1986;322(6082):831-4. doi: 10.1038/322831a0.
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Resistance of cytolytic lymphocytes to perforin-mediated killing. Murine cytotoxic T lymphocytes and human natural killer cells do not contain functional soluble homologous restriction factor or other specific soluble protective factors.溶细胞性淋巴细胞对穿孔素介导杀伤的抗性。小鼠细胞毒性T淋巴细胞和人类自然杀伤细胞不含功能性可溶性同源限制因子或其他特异性可溶性保护因子。
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Cell-mediated lysis of autologous platelets in chronic idiopathic thrombocytopenic purpura.慢性特发性血小板减少性紫癜中自体血小板的细胞介导溶解。
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IL-18 augments perforin-dependent cytotoxicity of liver NK-T cells.白细胞介素-18增强肝脏自然杀伤T细胞的穿孔素依赖性细胞毒性。
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Synergistic inhibition of human cell-mediated cytotoxicity by complement component antisera indicates that target cell lysis may result from an enzymatic cascade involving granzymes and perforin.补体成分抗血清对人细胞介导的细胞毒性的协同抑制表明,靶细胞裂解可能源于涉及颗粒酶和穿孔素的酶促级联反应。
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In vivo rejection of tumor cells dependent on CD8 cells that kill independently of perforin and FasL.体内肿瘤细胞的排斥反应依赖于不依赖穿孔素和FasL独立杀伤的CD8细胞。
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Molecular mechanisms of cytolysis by complement and by cytolytic lymphocytes.补体和细胞毒性淋巴细胞介导细胞溶解的分子机制。
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Increase in tumor necrosis factor-alpha mRNA but not perforin mRNA expression in response to two newly characterized anti-LFA-1 monoclonal antibodies.对两种新鉴定的抗淋巴细胞功能相关抗原-1单克隆抗体的应答中,肿瘤坏死因子-α信使核糖核酸表达增加,但穿孔素信使核糖核酸表达未增加。
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