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血清学可检测的组织相容性抗原在细胞介导的裂解诱导和效应步骤中的重要性。

The importance of serologically detectable histocompatibility antigens in the induction and effector step of cell-mediated lysis.

作者信息

Dennert G, Hyman R

出版信息

Eur J Immunol. 1977 May;7(5):251-7. doi: 10.1002/eji.1830070502.

DOI:10.1002/eji.1830070502
PMID:141372
Abstract

The induction and effector steps of T cell-mediated cytotoxicity (CMC) have been studied using a mouse tumor cell line and its variant, which is deficient in serologically defined (SD) H-2 antigens. In allogeneic mice the SDxcell line induces CMC, while the SD- cell line does not. However, both cell lines can be lysed by xenogeneic rat lymphocytes. Antiserum specific for rat T cells was used to demonstrate that CMC of both targetss is partially due to T cells. In allogeneic or syngeneic mouse systems the SD- cells coupled with the 2,4,6-trinitrophenyl (TNP) residue can neither induce CMC nor serve as targets for CMC, while TNP-coupled SDxcells can serve both as immunogen and as targets. Thus allogeneic or syngeneic mouse T cells do not interact with the TNP group of targets lacking H-2 SD antigens. However, mouse T killer cells sensitized to TNP-coupled cells may lyse TNP-coupled targets carrying different H-2 haplotypes. These experiments show that the induction and effector steps of CMC executed by mouse T cells, using TNP-coupled cells as immunogen or targets, need not necessarily demonstrate restriction with regard to a certain genetically defined H-2 haplotype. The presence of cell surface H-2 SD antigens is however, absolutely necessary for the induction and effector steps of CMC by mouse T cells. Using cold target inhibition assays, it was not possible to demonstrate recognition of the TNP moiety on TNP-coupled SDxcells.

摘要

利用一种小鼠肿瘤细胞系及其变体(该变体缺乏血清学定义的(SD)H-2抗原),对T细胞介导的细胞毒性(CMC)的诱导和效应步骤进行了研究。在同种异体小鼠中,SDx细胞系可诱导CMC,而SD-细胞系则不能。然而,两种细胞系均可被异种大鼠淋巴细胞裂解。使用针对大鼠T细胞的特异性抗血清来证明两种靶标的CMC部分归因于T细胞。在同种异体或同基因小鼠系统中,与2,4,6-三硝基苯基(TNP)残基偶联的SD-细胞既不能诱导CMC,也不能作为CMC的靶标,而TNP偶联的SDx细胞既可以作为免疫原,也可以作为靶标。因此,同种异体或同基因小鼠T细胞不与缺乏H-2 SD抗原的靶标的TNP基团相互作用。然而,对TNP偶联细胞致敏的小鼠T杀伤细胞可能会裂解携带不同H-2单倍型的TNP偶联靶标。这些实验表明,以TNP偶联细胞作为免疫原或靶标时,小鼠T细胞执行的CMC的诱导和效应步骤不一定表现出对某种基因定义的H-2单倍型的限制。然而,细胞表面H-2 SD抗原的存在对于小鼠T细胞进行CMC的诱导和效应步骤绝对必要。使用冷靶抑制试验,无法证明对TNP偶联的SDx细胞上的TNP部分有识别作用。

相似文献

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The importance of serologically detectable histocompatibility antigens in the induction and effector step of cell-mediated lysis.血清学可检测的组织相容性抗原在细胞介导的裂解诱导和效应步骤中的重要性。
Eur J Immunol. 1977 May;7(5):251-7. doi: 10.1002/eji.1830070502.
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引用本文的文献

1
The spatial relationship of the viral and H-2 antigens recognized by anti-viral CTLs.抗病毒 CTL 识别的病毒和 H-2 抗原的空间关系。
Immunogenetics. 1980;10(5):469-79. doi: 10.1007/BF01572582.
2
Cell-surface-antigen mutants of haematopoietic cells. Tools to study differentiation, biosynthesis and function.造血细胞的细胞表面抗原突变体。用于研究分化、生物合成和功能的工具。
Biochem J. 1985 Jan 1;225(1):27-40. doi: 10.1042/bj2250027.
3
Induction of cell-mediated cytotoxicity by lipoprotein containing histocompatibility antigens.含组织相容性抗原的脂蛋白诱导细胞介导的细胞毒性作用。
Immunology. 1979 Dec;38(4):757-63.
4
T-cell-mediated cytotoxic immune responses to F9 teratocarcinoma cells: cytolytic effector T cells lyse H-2-negative F9 cells and syngeneic spermatogonia.针对F9畸胎瘤细胞的T细胞介导的细胞毒性免疫反应:细胞溶解效应T细胞裂解H-2阴性的F9细胞和同基因精原细胞。
J Exp Med. 1978 Jan 1;147(1):251-64. doi: 10.1084/jem.147.1.251.
5
Participation of histocompatibility antigens in capping of molecularly independent cell surface components by their specific antibodies.组织相容性抗原通过其特异性抗体参与分子独立的细胞表面成分的帽化作用。
Proc Natl Acad Sci U S A. 1978 May;75(5):2406-10. doi: 10.1073/pnas.75.5.2406.
6
A role for elevated H-2 antigen expression in resistance to neoplasia caused by radiation-induced leukemia virus. Enhancement of effective tumor surveillance by killer lymphocytes.H-2抗原表达升高在抵抗辐射诱导的白血病病毒所致肿瘤形成中的作用。杀伤淋巴细胞增强有效的肿瘤监测。
J Exp Med. 1979 Apr 1;149(4):898-909. doi: 10.1084/jem.149.4.898.
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Increased synthesis and expression of H-2 antigens on thymocytes as a result of radiation leukemia virus infection: a possible mechanism for H-2 linked control of virus-induced neoplasia.辐射白血病病毒感染导致胸腺细胞上H-2抗原的合成与表达增加:H-2连锁控制病毒诱导肿瘤形成的一种可能机制。
J Exp Med. 1978 Feb 1;147(2):470-87. doi: 10.1084/jem.147.2.470.