INTRATHYMIC SELECTION OF MURINE TCR-ALPHA-BETA + CD4-CD8- THYMOCYTES
INTRATHYMIC SELECTION OF MURINE TCR-ALPHA-BETA + CD4-CD8- THYMOCYTES
复制标题
DOI：
10.1093/intimm/2.2.157
复制
发表时间：
1990-02-01
影响因子：
4.4
通讯作者：
SCOLLAY, R
中科院分区：
文献类型：
--
作者：
EGERTON, M;SCOLLAY, R
CD 4-CD 8-胸腺细胞群包含所有其他胸腺细胞的前体。然而，它也含有显著比例的表达表面TCR α的细胞。例如β，并且具有很少或没有前体活性。与外周T细胞一样，但与大多数其他胸腺细胞不同，这些TCR α。β + CD 4-CD 8-胸腺细胞不表达热稳定抗原。这些细胞的起源和发育状态都不清楚，这是本报告的主题。我们测量了MI s-1a与MI s-1b小鼠中TCR+ HSA-CD 4-CD 8-胸腺细胞中V β 8.1+细胞的比例，以确定它们是否经历了阴性选择。与成熟T细胞相比，这两种菌株的比例相似，表明它们及其前体都没有经历克隆缺失。我们还测量了这些细胞在动物早期生命中的积累，发现它非常缓慢。我们的数据还显示，尽管TCR-V β 8.1+细胞对与II类MHC相关的MI-1a具有反应性，但MI-1b小鼠中的大多数成熟TCR-V β 8.1+细胞是CD 8+，这表明与I类MHC具有额外的反应性。我们提出了TCR-V β 8.1+ CD 4-CD 8-胸腺细胞来源于TCR-V β 8.1+ CD 4 + CD 8+胸腺细胞的可能性，并且TCR-V β 8.1与I类和II类MHC的反应性导致了CD 4和CD 8的下调。
The CD4-CD8- thymocyte population contains the precursors of all other thymocytes. However, it also contains a significant proportion of cells which express surface TCR.alpha..beta., and have little or no precursor activity. Like peripheral T cells, but unlike most other thymocytes, these TCR.alpha..beta.+CD4-CD8- thymocytes do not express heat stable antigen. Both the origin and developmental status of these cells are unclear, and are the subject of this report. We have measured the proportion of V.beta.8.1+ cells amongst TCR+HSA-CD4-CD8- thymocytes in MIs-1a versus MIs-1b mice, in order to determine whether they have undergone negative selection. The proportions were similar in both strains, in contrast to mature T cells, indicating that neither they nor their precursors had undergone clonal deletion. We also measured the accumulation of these cells over the early life of the animal and found that it was extremely slow. Our data also show that although TCR-V.beta.8.1+ cells are reactive to MIs-1a in association with MHC class II, most mature TCR-V.beta.8.1+ cells in MIs-1b mice are CD8+, suggesting an additional reactivity with MHC class I. We raise the possibility that TCR-V.beta.8.1+ CD4-CD8- thymocytes are derived from TCR-V.beta.8.1+CD4+CD8+ thymocytes, and that the reactivity of TCR-V.beta.8.1 with both MHC classes I and II has resulted in the down-regulation of both CD4 and CD8.