Preclinical development of anti-CD21 chimeric antigen receptor T cells to treat T cell acute lymphoblastic leukemia

嵌合抗原受体 抗原 癌症研究 表位 T细胞 免疫疗法 免疫学 医学 生物 免疫系统
作者
Nicola Maciocia,Malika Hoekx,C. Calero Acuña,B Wade,Amy Burley,Saumya Ramanayake,Francesco Nannini,Patrycja Wawrzyniecka,Thaneswari Karpanasamy,M. Schuldt,Stephanie Ng,Mathieu Ferrari,Teresa Marafioti,Giuseppe Gritti,Shimobi Onuoha,David O’Connor,Lydia Lee,Marc R. Mansour,Asim Khwaja,Martin Pulé
出处
期刊:Science Translational Medicine [American Association for the Advancement of Science]
卷期号:17 (794): eadr1476-eadr1476
标识
DOI:10.1126/scitranslmed.adr1476
摘要

Patients with relapsed/refractory (r/r) T cell acute lymphoblastic leukemia (T-ALL) have a dismal prognosis, highlighting the urgent need for effective therapies. Chimeric antigen receptor (CAR)-T cell approaches targeting pan-T cell antigens may be limited by T cell aplasia and fratricide, necessitating "rescue" allogeneic hematopoietic stem cell transplantation. In this study, we identify CD21, a pan-B cell marker, as a promising target for T-ALL immunotherapy. CD21 is expressed in 50% of T-ALL cases at diagnosis but in fewer than 10% of mature T cells. We observed that CAR-T cells targeting membrane-distal CD21 epitopes were ineffective, likely because of the bulky, glycosylated nature of the antigen. However, when we engineered CAR-T cells to target membrane-proximal CD21 epitopes using an antigen-binding fragment (Fab)-CAR design, we demonstrated robust activity against T-ALL cell lines, primary tumors, and patient-derived xenografts in both in vitro and in vivo models. The enhanced efficacy of this Fab-CAR design was driven by its high stability and reduced surface expression, addressing limitations of traditional CAR constructs. In addition, pharmacological inhibition of the phosphatidylinositol 3-kinase axis up-regulated CD21 expression in T-ALL, further enhancing the potency of anti-CD21 CAR-T cells in vitro and in a patient-derived xenograft in vivo model. This study establishes CD21 as a viable CAR-T target and highlights advances in CAR design for bulky antigens, as well as the potential for pharmacological strategies to augment target expression. Anti-CD21 CAR-T cells represent a promising therapeutic option for improving outcomes for patients with T-ALL.
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
Nole应助浚稚采纳,获得10
刚刚
zzq应助浚稚采纳,获得10
刚刚
唐唐应助浚稚采纳,获得10
1秒前
苹果煎蛋发布了新的文献求助10
1秒前
JamesPei应助轻松铸海采纳,获得10
2秒前
3秒前
哭热发布了新的文献求助10
3秒前
长江长发布了新的文献求助10
3秒前
所所应助hesong采纳,获得10
3秒前
3秒前
剑影发布了新的文献求助10
4秒前
JamesPei应助111采纳,获得10
4秒前
英俊的铭应助智慧采纳,获得10
4秒前
拉长的远山完成签到,获得积分10
4秒前
5秒前
chao发布了新的文献求助10
5秒前
fcc完成签到 ,获得积分10
6秒前
平淡的忆之完成签到,获得积分10
6秒前
136542发布了新的文献求助10
7秒前
勒勒完成签到,获得积分10
7秒前
唠叨的代真完成签到,获得积分10
7秒前
苗条的钻石完成签到,获得积分10
7秒前
爱笑的山灵完成签到,获得积分10
8秒前
大头完成签到 ,获得积分10
8秒前
shenjj发布了新的文献求助10
9秒前
精明的大侠应助宋向荣采纳,获得20
9秒前
微笑谷雪应助Piena采纳,获得20
9秒前
snow完成签到 ,获得积分10
10秒前
10秒前
melens完成签到,获得积分10
10秒前
power完成签到,获得积分10
10秒前
10秒前
10秒前
11秒前
11秒前
不要预印本_注意着点完成签到,获得积分10
12秒前
打打应助faqiudexiaogou2采纳,获得10
12秒前
神勇马里奥完成签到 ,获得积分10
12秒前
13秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Arthritis and Related Conditions, An Issue of Orthopedic Clinics 1000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
ズームレンズの光学設計に関する研究 800
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 700
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7292168
求助须知:如何正确求助?哪些是违规求助? 8911140
关于积分的说明 18863722
捐赠科研通 6959278
什么是DOI,文献DOI怎么找? 3209566
关于科研通互助平台的介绍 2379066
邀请新用户注册赠送积分活动 2185369