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从人类T淋巴细胞受体的病理学到生理学

From pathology to physiology of the human T-lymphocyte receptor.

作者信息

Regueiro J R, Timón M, Pérez-Aciego P, Corell A, Martín-Vílla J M, Rodríguez-Gallego C, Góngora R, Arnaiz-Villena A

出版信息

Scand J Immunol. 1992 Sep;36(3):363-9. doi: 10.1111/j.1365-3083.1992.tb02950.x.

DOI:10.1111/j.1365-3083.1992.tb02950.x
PMID:1387725
Abstract

The recent description of a selective human CD3 gamma deficiency and other T-cell receptor (TCR)/CD3 structural and functional defects, together with previous biochemical data on the structure and interactions of the TCR/CD3 complex, may aid in elucidating the physiology of this multi-subunit membrane ensemble. CD3 gamma seemed to be required for the commitment and thymic maturation of an important fraction of T lymphocytes to the CD8 (but not CD4) lineage, perhaps by participating with the CD8 co-receptor in the instructive signal delivered through the alpha beta TCR during intrathymic positive selection by HLA class I molecules. The homologous CD3 delta component would, in contrast, be necessary for the selection of CD4 lymphocytes by HLA class II molecules. The interaction of CD4 and CD8 with the TCR/CD3 complex during antigen recognition may thus be asymmetrical, taking place through CD3 delta and gamma, respectively. Also, the existence of in vivo functional TCR/CD3 hemireceptors (lacking either CD3 gamma or CD3 delta) is suggested, and defects in their relative amount on the T-cell surface may disrupt unresponsiveness to self antigens and generate autoimmunity.

摘要

最近对选择性人类CD3γ缺陷以及其他T细胞受体(TCR)/CD3结构和功能缺陷的描述,连同先前关于TCR/CD3复合物结构和相互作用的生化数据,可能有助于阐明这种多亚基膜组件的生理学。CD3γ似乎是T淋巴细胞中很大一部分向CD8(而非CD4)谱系定向分化和胸腺成熟所必需的,可能是通过在HLA I类分子进行胸腺内阳性选择期间,与CD8共受体一起参与通过αβ TCR传递的指导性信号。相比之下,同源的CD3δ成分对于HLA II类分子选择CD4淋巴细胞是必需的。因此,在抗原识别过程中,CD4和CD8与TCR/CD3复合物的相互作用可能是不对称的,分别通过CD3δ和γ发生。此外,提示存在体内功能性TCR/CD3半受体(缺乏CD3γ或CD3δ),并且它们在T细胞表面的相对数量缺陷可能会破坏对自身抗原的无反应性并产生自身免疫。

相似文献

1
From pathology to physiology of the human T-lymphocyte receptor.从人类T淋巴细胞受体的病理学到生理学
Scand J Immunol. 1992 Sep;36(3):363-9. doi: 10.1111/j.1365-3083.1992.tb02950.x.
2
T lymphocyte signalling defects and immunodeficiency due to the lack of CD3 gamma.由于缺乏CD3γ导致的T淋巴细胞信号缺陷和免疫缺陷。
Immunodeficiency. 1993;4(1-4):121-9.
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Patterns of membrane TcR alpha beta and TcR gamma delta chain expression by normal blood CD4+CD8-, CD4-CD8+, CD4-CD8dim+ and CD4-CD8- lymphocytes.正常血液中CD4+CD8-、CD4-CD8+、CD4-CD8dim+和CD4-CD8-淋巴细胞的膜TcRαβ和TcRγδ链表达模式
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Structural comparison of alpha/beta and gamma/delta T cell receptor-CD3 complexes reveals identical subunit interactions but distinct cross-linking patterns of T cell receptor chains.α/β和γ/δ T细胞受体-CD3复合物的结构比较揭示了相同的亚基相互作用,但T细胞受体链的交联模式不同。
Eur J Immunol. 1990 Sep;20(9):2105-11. doi: 10.1002/eji.1830200932.
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Patterns of costimulation of T cell clones by cross-linking CD3, CD4/CD8, and class I MHC molecules.通过交联CD3、CD4/CD8和I类MHC分子对T细胞克隆进行共刺激的模式。
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Immunoregulatory function of CD3+, CD4-, and CD8- T cells. Gamma delta T cell receptor-positive T cells from nude mice abrogate oral tolerance.CD3 +、CD4 - 和CD8 - T细胞的免疫调节功能。来自裸鼠的γδT细胞受体阳性T细胞消除口服耐受性。
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Characterization and expression of the human T cell receptor-T3 complex by monoclonal antibody F101.01.利用单克隆抗体F101.01对人T细胞受体-T3复合物进行表征及表达研究
Scand J Immunol. 1988 Jun;27(6):685-96. doi: 10.1111/j.1365-3083.1988.tb02402.x.
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Alpha/beta heterodimeric T-cell receptor expression early in thymocyte differentiation.α/β异二聚体T细胞受体在胸腺细胞分化早期的表达。
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Signal transduction via CD4, CD8, and CD28 in mature and immature thymocytes. Implications for thymic selection.成熟和未成熟胸腺细胞中通过CD4、CD8和CD28进行的信号转导。对胸腺选择的影响。
J Immunol. 1991 Mar 1;146(5):1428-36.
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Regulatory function for murine intraepithelial lymphocytes. Two subsets of CD3+, T cell receptor-1+ intraepithelial lymphocyte T cells abrogate oral tolerance.小鼠上皮内淋巴细胞的调节功能。CD3+、T细胞受体-1+上皮内淋巴细胞T细胞的两个亚群可消除口服耐受性。
J Immunol. 1990 Oct 1;145(7):2010-9.

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Primary T lymphocyte immunodeficiency associated with a selective impairment of CD2, CD3, CD43 (but not CD28)-mediated signal transduction.原发性T淋巴细胞免疫缺陷与CD2、CD3、CD43(而非CD28)介导的信号转导选择性受损相关。
Clin Exp Immunol. 1994 Sep;97(3):386-91. doi: 10.1111/j.1365-2249.1994.tb06099.x.