Expression of T-cell receptors TcR1 (gamma/delta) and TcR2 (alpha/beta) in the human intestinal mucosa.

Expression of T-cell receptors TcR1 (gamma/delta) and TcR2 (alpha/beta) in the human intestinal mucosa.
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T 细胞受体 TcR1(γ/δ)和 TcR2(α/β)在人肠粘膜中的表达。

DOI:
10.1007/978-94-009-1848-1_17
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发表时间:
1989
期刊:
影响因子:
6.4
通讯作者:
A. Boylston
A. Boylston
中科院分区:
医学2区
文献类型:
--
作者:
L. Trejdosiewicz;C. Smart;D. Oakes;P. Howdle;G. Malizia;D. Campana;A. Boylston

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用抗CD 3、CD 4、CD 8、CD 5和CD 6的抗体,以及分别抗T细胞受体(TcR)TcR 2(α/β)和TcR 1(γ/δ)β链和δ链的抗体β F1和TCR δ 1,通过双标记免疫荧光研究了正常成人胃肠道粘膜的冷冻切片。在固有层内几乎没有发现TcR 1+。在上皮隔室中,TcR 1+细胞不常见:在小肠中,TcR 1 + T细胞占2%。在结肠上皮中,表达γ/δ-链的T细胞的百分比较高,平均值接近15- 20%,尽管与小肠相比这种明显较大的百分比增加部分反映了结肠IEL的低得多的密度,因为TCR δ 1+细胞的绝对数量相当。在TcR 1+人群中,约一半为CD 4-CD 8-(“双阴性”),其余为CD 8+。TcR 1+细胞也是CD 5-CD 6-,与CD 8的表达无关。未观察到表达TcR 1的CD 4+细胞:基本上所有CD 4+细胞均为β F1+,标记强度存在一定差异。大约30-50%的CD 8+亚群强烈表达β F1抗原。然而,在其余的TcR 1-CD 8+细胞(均为CD 5-CD 6-表型)中,仅当链霉亲和素和生物素偶联物用于扩增标记时,才可检测到β F1抗原的表达。因此,CD 8 + CD 5-亚群,小肠上皮细胞室的一个突出的群体,要么是TcR 2迟钝的大多数或TcR 1+的少数。我们的数据表明,γ/δ TcR 1细胞可能被积极排除在肠固有层之外,并且确实发生的任何优先定位都是有限的,而是结肠粘膜的特征,而不是小肠。
Cryostat sections of normal human adult gastrointestinal mucosae were studied by double-label immunofluorescence with antibodies to CD3, CD4, CD8, CD5 and CD6, in parallel with antibodies beta F1 and TCR delta 1 against beta-chains and delta-chains of the T-cell receptor (TcR) types TcR2 (alpha/beta) and TcR1 (gamma/delta), respectively. Virtually no TcR1+ were found within the lamina propria. In the epithelial compartment, TcR1+ cells were infrequent: in the small bowel, congruent to 2% of T cells were TcR1+. In the colonic epithelium, the percentage of T cells expressing gamma/delta-chains was higher, with a mean value approximating 15-20%, although this apparently large percentage increase compared with small bowel reflects in part a much lower density of colonic IEL, as absolute numbers of TCR delta 1+ cells were comparable. Of the TcR1+ population, about half were CD4- CD8-, 'double negatives' and the remainder were CD8+. TcR1+ cells were also CD5- CD6-, irrespective of expression of CD8. No CD4+ cells expressing TcR1 were observed: essentially all CD4+ cells were beta F1+, with some variability of labelling intensity. Approximately 30-50% of the CD8+ subset expressed the beta F1 antigen strongly. However, in the remaining TcR1- CD8+ cells, which were all of the CD5- CD6- phenotype, expression of the beta F1 antigen was only detectable when streptavidin and biotin conjugates were used for amplification of labelling. Thus, the CD8+ CD5- subset, a prominent population of the epithelial compartment of the small bowel, was either TcR2dull in the majority or TcR1+ in a minority. Our data imply that gamma/delta TcR1 cells may be actively excluded from intestinal lamina propria, and that any preferential localization that does occur is limited and is rather a feature of the colonic mucosa, rather than the small bowel.