Cancer immunotherapy with check point inhibitor can cause autoimmune adverse events due to loss of Treg homeostasis

易普利姆玛 无容量 自身免疫 免疫学 医学 免疫系统 免疫疗法 癌症免疫疗法 免疫检查点 银耳霉素 癌症 内科学
作者
Prabhakaran Kumar,Shikha Saini,Bellur S. Prabhakar
出处
期刊:Seminars in Cancer Biology [Elsevier]
卷期号:64: 29-35 被引量:93
标识
DOI:10.1016/j.semcancer.2019.01.006
摘要

Regulatory T-cells (Tregs) can facilitate immune evasion by tumor cells by dampening anti-tumor immunity. Reduced Teff/Treg ratio and enhanced Treg functional activity have been observed in patients suffering from different types of cancers, and attenuated Treg numbers/functions can serve as prognostic indicators. Normally, Tregs play an essential role in the maintenance of immune tolerance and prevention of autoimmunity. The most common immune checkpoint blockers (ICB) targeting co-inhibitory receptors such as anti-CTLA4 (ipilimumab and tremelimumab) and anti-PD1 (pembrolizumab and nivolumab)/anti-PD-L1 (atezolizumab) have achieved unprecedented success in cancer treatment by facilitating an effective anti-tumor immune response, at least in part, by blocking Treg mediated immunosuppression. While ICBs have shown remarkable success in cancer immunotherapy, immune-related adverse events (IRAEs) arising from ICB have forced consideration of ways to maintain immune homeostasis post ICB treatment. Preclinical models of IRAEs have shown a negative correlation between Treg numbers and IRAEs. Therefore, understanding the "ying-yang" role of Tregs in the regulation of autoimmunity and anti-tumor immunity is critical to provoking an effective anti-tumor response while maintaining immune homeostasis. Studies aimed at developing effective approaches to minimize IRAEs without compromising anti-tumor immunity are underway. Herein, we discuss 1) the critical role of key co-inhibitory receptors on Treg homeostasis and tumor tolerance; 2) how co-receptor blockade by cancer immunotherapy can lead to autoimmune adverse events; and 3) recently emerging management strategies to minimize autoimmune adverse events arising from ICB.
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
刚刚
丘比特应助这课题真顺利采纳,获得10
3秒前
慕青应助留胡子的以柳采纳,获得10
3秒前
文昱发布了新的文献求助10
4秒前
4秒前
6秒前
期刊应助科研通管家采纳,获得10
7秒前
CipherSage应助科研通管家采纳,获得10
7秒前
思源应助科研通管家采纳,获得10
7秒前
CHENXIUWEN应助科研通管家采纳,获得10
7秒前
Owen应助科研通管家采纳,获得10
7秒前
今后应助科研通管家采纳,获得10
7秒前
田様应助科研通管家采纳,获得10
7秒前
无餍应助科研通管家采纳,获得10
7秒前
研友_VZG7GZ应助科研通管家采纳,获得10
7秒前
隐形曼青应助科研通管家采纳,获得10
7秒前
SciGPT应助科研通管家采纳,获得10
7秒前
8R60d8应助科研通管家采纳,获得10
7秒前
无花果应助科研通管家采纳,获得10
7秒前
领导范儿应助科研通管家采纳,获得10
7秒前
打打应助科研通管家采纳,获得10
7秒前
NexusExplorer应助老木虫采纳,获得10
8秒前
Galri完成签到 ,获得积分10
8秒前
11关注了科研通微信公众号
9秒前
11秒前
兼雨梧桐应助桃桃杨乐多采纳,获得10
11秒前
Owen应助卡皮巴拉采纳,获得10
12秒前
12秒前
南雪既白完成签到,获得积分10
12秒前
小二郎应助xuhailong采纳,获得10
13秒前
13秒前
Doublelin完成签到,获得积分10
14秒前
15秒前
乔乐发布了新的文献求助10
15秒前
不安青牛应助调皮的鬼神采纳,获得10
16秒前
怕孤独的海秋完成签到,获得积分20
16秒前
16秒前
月青悠发布了新的文献求助10
17秒前
wuuu_ruby完成签到,获得积分10
17秒前
17秒前
高分求助中
Production Logging: Theoretical and Interpretive Elements 2500
Востребованный временем 2500
Aspects of Babylonian celestial divination : the lunar eclipse tablets of enuma anu enlil 1500
Agaricales of New Zealand 1: Pluteaceae - Entolomataceae 1040
Healthcare Finance: Modern Financial Analysis for Accelerating Biomedical Innovation 1000
Classics in Total Synthesis IV: New Targets, Strategies, Methods 1000
지식생태학: 생태학, 죽은 지식을 깨우다 600
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 3459163
求助须知:如何正确求助?哪些是违规求助? 3053710
关于积分的说明 9037991
捐赠科研通 2742977
什么是DOI,文献DOI怎么找? 1504606
科研通“疑难数据库(出版商)”最低求助积分说明 695334
邀请新用户注册赠送积分活动 694663