Fas Ligand–Positive Membranous Vesicles Isolated from Sera of Patients with Oral Cancer Induce Apoptosis of Activated T Lymphocytes

Fas配体 微泡 微泡 Jurkat细胞 细胞凋亡 生物 分子生物学 癌症研究 免疫学 细胞生物学 T细胞 程序性细胞死亡 免疫系统 生物化学 小RNA 基因
作者
Jeong Whun Kim,Eva Wieckowski,Douglas D. Taylor,Torsten E. Reichert,Simon C. Watkins,Theresa L. Whiteside
出处
期刊:Clinical Cancer Research [American Association for Cancer Research]
卷期号:11 (3): 1010-1020 被引量:470
标识
DOI:10.1158/1078-0432.1010.11.3
摘要

In patients with oral squamous cell carcinoma, a high proportion of T cells in the tumor undergo apoptosis, which correlates with Fas ligand (FasL) expression on tumor cells. The present study was done to identify mechanisms responsible for apoptosis of T cells seen in the peripheral circulation of these patients.Sera of 27 patients, normal donor sera, and supernatants of cultured normal or tumor cells were fractionated by size exclusion chromatography and ultracentrifugation to isolate microvesicles. The presence of microvesicle-associated FasL was studied by Western blots, blocking with anti-Fas reagents, and immunoelectron microscopy. Biological activities of microvesicles were tested including the ability to induce apoptosis of Jurkat and T-cell blasts. Semiquantitative analysis of FasL in microvesicles was correlated with caspase-3 activity, DNA fragmentation, cytochrome c release, loss of mitochondrial membrane potential, and TCR-zeta chain expression in lymphocytes.FasL-positive (FasL+) microvesicles were detected in sera of 21 of 27 patients. Microvesicles contained 42 kDa FasL. These microvesicles induced caspase-3 cleavage, cytochrome c release, loss of mitochondrial membrane potential, and reduced TCR-zeta chain expression in target lymphocytes. Biological activity of the FasL+ microvesicles was partially blocked by ZB4 anti-Fas monoclonal antibody. Microvesicle-associated FasL levels correlated with the patients' tumor burden and nodal involvement.Sera of patients with active oral squamous cell carcinoma contain FasL+ microvesicles, which induce the receptor and mitochondrial apoptotic pathways in Jurkat and activated T cells.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
zpbb完成签到,获得积分10
刚刚
1秒前
1秒前
zxcvbnm完成签到 ,获得积分10
1秒前
fanfan完成签到,获得积分10
1秒前
zhuiyu完成签到,获得积分10
2秒前
李白完成签到,获得积分10
2秒前
等待凡波完成签到 ,获得积分10
2秒前
KevinL完成签到,获得积分10
3秒前
3秒前
JIE完成签到,获得积分10
3秒前
3秒前
Accept完成签到,获得积分10
4秒前
阿翼完成签到 ,获得积分10
4秒前
brd完成签到,获得积分10
4秒前
optical完成签到,获得积分10
4秒前
5秒前
好多鱼完成签到,获得积分10
5秒前
bkagyin应助乐观的西装采纳,获得10
5秒前
Annora发布了新的文献求助10
5秒前
生动初蓝发布了新的文献求助10
6秒前
甲乙丙丁发布了新的文献求助10
6秒前
Glngar完成签到,获得积分10
6秒前
汉中太守魏延完成签到,获得积分10
6秒前
CodeCraft应助KevinL采纳,获得10
6秒前
gene完成签到 ,获得积分10
6秒前
chan完成签到,获得积分10
6秒前
大个应助fuchao采纳,获得10
7秒前
7秒前
影子123完成签到,获得积分20
7秒前
happiness完成签到 ,获得积分10
7秒前
7秒前
8秒前
wwba完成签到,获得积分10
8秒前
CHSLN完成签到 ,获得积分10
8秒前
吴晗硕查文献完成签到 ,获得积分10
8秒前
卡卡卡发布了新的文献求助10
9秒前
QQQ完成签到,获得积分10
9秒前
ooseabiscuit完成签到,获得积分10
10秒前
星辰大海应助成就的曼梅采纳,获得10
10秒前
高分求助中
Genetics: From Genes to Genomes 3000
Production Logging: Theoretical and Interpretive Elements 2500
Continuum thermodynamics and material modelling 2000
Healthcare Finance: Modern Financial Analysis for Accelerating Biomedical Innovation 2000
Applications of Emerging Nanomaterials and Nanotechnology 1111
Les Mantodea de Guyane Insecta, Polyneoptera 1000
Diabetes: miniguías Asklepios 800
热门求助领域 (近24小时)
化学 医学 材料科学 生物 工程类 有机化学 生物化学 纳米技术 内科学 物理 化学工程 计算机科学 复合材料 基因 遗传学 物理化学 催化作用 细胞生物学 免疫学 电极
热门帖子
关注 科研通微信公众号,转发送积分 3471793
求助须知:如何正确求助?哪些是违规求助? 3064675
关于积分的说明 9089704
捐赠科研通 2755407
什么是DOI,文献DOI怎么找? 1512031
邀请新用户注册赠送积分活动 698629
科研通“疑难数据库(出版商)”最低求助积分说明 698517