Analysis of the susceptibility of CD57+ T cells to CD3-mediated apoptosis

Author:

Shinomiya N1,Koike Y2,Koyama H3,Takayama E4,Habu Y1,Fukasawa M1,Tanuma S3,Seki S1

Affiliation:

1. Departments of Microbiology

2. Pediatrics

3. Department of Biochemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Tokyo, Japan

4. Parasitology, National Defense Medical College, Tokorozawa, Japan

Abstract

Summary After stimulation with anti-CD3 antibody in vitro, CD57+ T cells showed a greater susceptibility to apoptosis than CD57–αβT cell receptor (TCR)+ T cells (regular αβ T cells). The apoptotic fraction of CD57+ T cells showed an increased production of active caspase-3. An increase in both Fas expression and Fas-ligand (FasL) production was also observed in CD57+ T cells, whereas the expression of survivin was suppressed in CD57+ T cells compared to that of regular αβ T cells. CD57+ T cells display a biased expansion of a few Vβ T cell fractions in individuals, but such Vβ T cells were not specifically susceptible to CD3-mediated apoptosis. The TCR expression level of CD57+ T cells was much lower than that of regular T cells and anti-TCR antibody stimulation induced a smaller apoptotic proportion of CD57+ T cells than did anti-CD3 antibody. Although the CD3ɛ expression levels were similar in both T cell subsets, the CD3ζ level of CD57+ T cells was significantly higher than that of regular T cells. These results suggest that several apoptotic and anti-apoptotic molecules are involved in the CD3-induced apoptosis of CD57+ T cells and raise the possibility that the imbalance in expression of the CD3ɛ and CD3ζ chains may also contribute to the susceptibility of CD57+ T cells to undergo apoptosis.

Publisher

Oxford University Press (OUP)

Subject

Immunology,Immunology and Allergy

Cited by 9 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3