PD-L1+ neutrophils mediate immune regulation of CD8+ T cells in halo nevi

白癜风 CD8型 免疫系统 免疫学 发病机制 黑素细胞 光环 黑色素瘤 医学 癌症研究 生物 量子力学 银河系 物理
作者
Yixuan Zhang,Yingying Xu,Wenjun Cui,Haoyang Wang,Min Li,Lu Liu
出处
期刊:Frontiers in Immunology [Frontiers Media SA]
卷期号:16: 1628913-1628913
标识
DOI:10.3389/fimmu.2025.1628913
摘要

Background Halo nevi are clinically common and are characterized by a circle of leukoderma around the central melanocytic nevus. Studies have shown that the pathogenesis of halo nevi is similar to that of vitiligo and is associated with the role of CD8⁺ T lymphocytes in melanocyte destruction. Histopathological findings have revealed neutrophil infiltration in halo nevi; however, the specific immune mechanisms involving neutrophils have not been thoroughly investigated. In the present study, we investigated the role of neutrophils in halo nevi using histopathological and immunological analyses. Methods To this end, we examined the infiltration patterns of immune cells in halo nevi, with a particular focus on IFN-γ-induced PD-L1 expression in neutrophils and its potential immunoregulatory effects. Results The results demonstrated that IFN-γ expression in the lesional skin of halo nevi contributed to the induction of PD-L1 expression in neutrophils. PD-L1⁺ neutrophils promoted apoptosis and suppressed the function of CD8⁺ T lymphocytes. Notably, some halo nevi showed a tendency to spontaneous regression, but the underlying mechanisms remain unclear, and this regulatory mechanism influences the local immune response and may facilitate the repigmentation of the surrounding leukoderma in halo nevi. Conclusions This study is the first to explore the involvement of neutrophils in halo nevi and reveal the potential immunoregulatory role of PD-L1 in this process. The elucidation of this mechanism not only provides a more comprehensive understanding of autoimmune skin diseases but may also offer new strategies for targeted therapy in other related disorders, such as vitiligo.
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
斯文败类应助syr采纳,获得10
刚刚
iHateTheWorld完成签到,获得积分10
刚刚
量子星尘发布了新的文献求助10
刚刚
无限绮南发布了新的文献求助10
刚刚
1秒前
2秒前
2秒前
2秒前
2秒前
从容甜瓜完成签到,获得积分0
3秒前
4秒前
yingying发布了新的文献求助10
4秒前
二掌柜发布了新的文献求助10
4秒前
4秒前
David应助科研通管家采纳,获得10
5秒前
小白发布了新的文献求助10
6秒前
6秒前
NexusExplorer应助shaw采纳,获得10
6秒前
斯文败类应助科研通管家采纳,获得10
6秒前
科研通AI6应助科研通管家采纳,获得10
6秒前
我是老大应助科研通管家采纳,获得10
6秒前
6秒前
6秒前
无奈zzz关注了科研通微信公众号
6秒前
核桃发布了新的文献求助10
6秒前
天天快乐应助科研通管家采纳,获得10
6秒前
iNk应助科研通管家采纳,获得10
7秒前
David应助科研通管家采纳,获得10
7秒前
David应助科研通管家采纳,获得10
7秒前
7秒前
斯文败类应助科研通管家采纳,获得10
7秒前
科研通AI6应助科研通管家采纳,获得10
7秒前
iNk应助科研通管家采纳,获得10
7秒前
我是老大应助科研通管家采纳,获得10
7秒前
7秒前
7秒前
7秒前
7秒前
7秒前
高分求助中
2025-2031全球及中国金刚石触媒粉行业研究及十五五规划分析报告 40000
(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
Introduction to strong mixing conditions volume 1-3 5000
Agyptische Geschichte der 21.30. Dynastie 3000
Les Mantodea de guyane 2000
Clinical Microbiology Procedures Handbook, Multi-Volume, 5th Edition 2000
„Semitische Wissenschaften“? 1510
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 计算机科学 有机化学 物理 生物化学 纳米技术 复合材料 内科学 化学工程 人工智能 催化作用 遗传学 数学 基因 量子力学 物理化学
热门帖子
关注 科研通微信公众号,转发送积分 5749029
求助须知:如何正确求助?哪些是违规求助? 5456131
关于积分的说明 15362419
捐赠科研通 4888546
什么是DOI,文献DOI怎么找? 2628508
邀请新用户注册赠送积分活动 1576865
关于科研通互助平台的介绍 1533626