1F7 (CD26): a marker of thymic maturation involved in the differential regulation of the CD3 and CD2 pathways of human thymocyte activation.

1F7 (CD26): a marker of thymic maturation involved in the differential regulation of the CD3 and CD2 pathways of human thymocyte activation.
复制标题

DOI:
10.4049/jimmunol.147.9.2825
复制
发表时间:
1991-11
影响因子:
4.4
通讯作者:
Nam H. Dang;Y. Torimoto;K. Shimamura;Takashi Tanaka;Jennifer Daley;S. F. Schlossman;Chikao Morimoto
Nam H. Dang;Y. Torimoto;K. Shimamura;Takashi Tanaka;Jennifer Daley;S. F. Schlossman;Chikao Morimoto
中科院分区:
医学2区
文献类型:
--
作者:
Nam H. Dang;Y. Torimoto;K. Shimamura;Takashi Tanaka;Jennifer Daley;S. F. Schlossman;Chikao Morimoto

文献摘要

相似文献

我们最近表明,固相固定化的抗1F 7识别110 kDa的CD 26 Ag是通过CD 3和CD 2途径的人外周血T细胞活化的共致性。我们还证明了抗1F 7的结合导致CD 26表面表达的消失,并且这种抗1F 7诱导的调节导致抗CD 3或抗CD 2介导的外周血T细胞活化的增加。在这份报告中,我们通过研究1F 7在人胸腺细胞活化的CD 3和CD 2途径上的表达和功能关系来扩展这些发现。我们现在证明,大多数的抗1F 7反应是在髓质胸腺细胞,胸腺细胞表达高水平的CD 3(CD 3 H)的人口。我们还表明,抗1F 7抗体的结合可诱导CD 26表面表达的降低,而对CD 3或CD 2的表面表达没有可检测的影响。最重要的是,我们发现固相固定的抗1F 7抗体对抗CD 3抗体诱导的胸腺细胞活化具有协同作用,但对抗CD 2抗体诱导的胸腺细胞活化没有协同作用。此外,抗1F 7诱导的CD 26调节导致CD 3介导的而非CD 2介导的人胸腺细胞活化增强。所观察到的CD 26对CD 3/TCR活化途径的功能性影响主要限于成熟胸腺细胞,其特征在于CD 5的高表面表达,尽管CD 26在表达低水平CD 5的细胞上也与CD 3/TCR途径功能性相关。证明CD 26参与调节人胸腺细胞活化主要限于CD 3途径,不像其参与成熟外周血T淋巴细胞活化的CD 3和CD 2途径,因此我们的数据表明,CD 26可能通过CD 3途径的差异参与在胸腺分化和成熟中发挥作用。
We have recently shown that solid-phase immobilization of anti-1F7 recognizing the 110-kDa CD26 Ag is comitogenic for human peripheral blood T cell activation via both the CD3 and CD2 pathways. We have also demonstrated that binding of anti-1F7 leads to the disappearance of CD26 surface expression, and this anti-1F7-induced modulation results in an increase in anti-CD3 or anti-CD2-mediated peripheral blood T cell activation. In this report, we extended these findings by examining the expression and functional relationship of 1F7 on the CD3 and CD2 pathways of activation of human thymocytes. We now demonstrated that most of the anti-1F7 reactivity is found on medullary thymocytes, the population of thymocytes expressing high level of CD3 (CD3H). We have also shown that binding of anti-1F7 can induce a decrease in CD26 surface expression, with no detectable effect on the surface expression of CD3 or CD2. Most importantly, we showed that solid-phase immobilization of anti-1F7 has a comitogenic effect on thymocyte activation induced by anti-CD3 but not anti-CD2. In addition, anti-1F7-induced modulation of CD26 results in an enhancement in CD3-mediated but not CD2-mediated human thymocyte activation. The observed functional effect of CD26 on the CD3/TCR pathway of activation is mainly restricted to mature thymocytes as distinguished by high surface expression of CD5, although CD26 is also functionally associated with the CD3/TCR pathway on cells expressing low level of CD5. Demonstrating that CD26 involvement in the regulation of human thymocyte activation is restricted mainly to the CD3 pathway, unlike its involvement with both the CD3 and CD2 pathways of mature peripheral blood T lymphocyte activation, our data hence suggested that CD26 may play a role in thymic differentiation and maturation via the differential engagement of the CD3 pathway.