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细菌超抗原在小鼠严重联合免疫缺陷-人肝脏/胸腺模型中介导T细胞缺失。

Bacterial superantigens mediate T cell deletions in the mouse severe combined immunodeficiency-human liver/thymus model.

作者信息

Baccala R, Vandekerckhove B A, Jones D, Kono D H, Roncarolo M G, Theofilopoulos A N

机构信息

Department of Immunology, Scripps Research Institute, La Jolla, California 92037.

出版信息

J Exp Med. 1993 May 1;177(5):1481-5. doi: 10.1084/jem.177.5.1481.

Abstract

The ability to analyze T cell receptor (TCR) thymic repertoire shaping in humans by self and foreign ligands is hampered by the lack of suitable models. We recently documented that the mouse severe combined immunodeficiency (SCID)-human fetal liver/thymus model recapitulates the TCR V beta gene repertoire of human thymocytes. Here, we show that an exogenous superantigen, staphylococcal enterotoxin B, administered to such mice induces clonal deletions in both CD4+8- and CD8+4- cells involving the same human V beta clones that are selected in vitro by this toxin. This model, therefore, may allow comprehensive studies into the effects of microbial and other agents on human T cell thymic selection processes in a biologically relevant setting.

摘要

由于缺乏合适的模型,分析人类T细胞受体(TCR)胸腺库在自身和外来配体作用下形成的能力受到了阻碍。我们最近记录到,小鼠严重联合免疫缺陷(SCID)-人胎儿肝脏/胸腺模型能够重现人类胸腺细胞的TCR Vβ基因库。在此,我们表明,给这类小鼠施用外源性超抗原——葡萄球菌肠毒素B,会在CD4+8-和CD8+4-细胞中诱导克隆性缺失,涉及该毒素在体外选择的相同人类Vβ克隆。因此,该模型可能有助于在生物学相关环境中全面研究微生物和其他因子对人类T细胞胸腺选择过程的影响。

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The staphylococcal enterotoxins and their relatives.葡萄球菌肠毒素及其相关毒素。
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