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人胸腺上皮细胞瘤中缺乏CD69的未成熟CD3-CD4+CD8-单阳性细胞的积累。

Accumulation of immature CD3-CD4+CD8- single-positive cells that lack CD69 in epithelial cell tumors of the human thymus.

作者信息

Takeuchi Y, Fujii Y, Okumura M, Inada K, Nakahara K, Matsuda H

机构信息

First Department of Surgery, Osaka University Medical School, Japan.

出版信息

Cell Immunol. 1995 Apr 1;161(2):181-7. doi: 10.1006/cimm.1995.1025.

Abstract

Human thymomas are epithelial tumors that are associated with a large number of nonneoplastic T cells of mainly immature phenotype, suggesting that epithelial cells of thymomas retain the function of thymic cortical epithelium. We report here that a large proportion (16-85%, mean +/- SD 58 +/- 22%, n = 17) of CD4+ single-positive T cells within the thymoma lack cell surface expression of CD3 and also of CD69, an early activation antigen that is expressed by positively selected thymocytes. Normal thymus had this CD4+CD8-CD3- population at much lower levels (12 +/- 7%, n = 11). It has been reported that in the human the CD4+CD8-CD3- cells are the predominant population that is intermediate between the CD4-CD8- double-negative and CD4+CD8+ double-positive stages. In contrast to CD4+ single-positive cells, most of the CD8+ single-positive cells in the thymoma as well as in the normal thymus expressed CD69 and a high level of CD3. A partial explanation of these observations is that the epithelial cells of thymoma were unable to positively select all the immature thymocytes generated in the thymoma. This relative inefficiency of positive selection could not be attributed solely to the paucity of MHC class II expression in the thymoma.

摘要

人类胸腺瘤是上皮性肿瘤,与大量主要为未成熟表型的非肿瘤性T细胞相关,这表明胸腺瘤的上皮细胞保留了胸腺皮质上皮的功能。我们在此报告,胸腺瘤内很大一部分(16 - 85%,平均±标准差58±22%,n = 17)CD4 +单阳性T细胞缺乏CD3以及CD69的细胞表面表达,CD69是一种由阳性选择的胸腺细胞表达的早期激活抗原。正常胸腺中这种CD4 + CD8 - CD3 - 细胞群体的水平要低得多(12±7%,n = 11)。据报道,在人类中,CD4 + CD8 - CD3 - 细胞是CD4 - CD8 - 双阴性和CD4 + CD8 + 双阳性阶段之间的主要中间群体。与CD4 +单阳性细胞不同,胸腺瘤以及正常胸腺中的大多数CD8 +单阳性细胞表达CD69和高水平的CD3。对这些观察结果的部分解释是,胸腺瘤的上皮细胞无法对胸腺瘤中产生的所有未成熟胸腺细胞进行阳性选择。这种阳性选择的相对低效不能仅仅归因于胸腺瘤中MHC II类表达的缺乏。

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