• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

斑秃发病机制中以巨噬细胞为中心的免疫代谢串扰:机制与治疗意义

Macrophage-Centric Immunometabolic Crosstalk in Alopecia Areata Pathogenesis: Mechanisms and Therapeutic Implications.

作者信息

Liu Xu, Song Xiuzu

机构信息

Department of Dermatology, Hangzhou Third People's Hospital, West Lake Ave 38, Hangzhou, 310009, People's Republic of China.

出版信息

Clin Rev Allergy Immunol. 2025 May 22;68(1):50. doi: 10.1007/s12016-025-09060-3.

DOI:10.1007/s12016-025-09060-3
PMID:40405030
Abstract

Although alopecia areata (AA) is recognized as a hair loss disorder stemming from the dysregulation of cutaneous immune homeostasis, its precise pathogenesis still remains elusive. The collapse of hair follicle (HF) immune privilege (IP), leading to immune cell-mediated attack on the hair follicle, is currently the widely accepted fundamental mechanism of AA. Among the immune cells studied in this context, CD8 T cells and regulatory T (Treg) cells are relatively well-researched, but the direct involvement of macrophages in the disease process has been less frequently demonstrated. In this review, we summarize various previous studies on macrophages and hypothesize the immune mechanisms by which macrophages contribute to the pathogenesis of AA. This exploration provides new insights for future research and potential clinical treatments.

摘要

尽管斑秃(AA)被认为是一种源于皮肤免疫稳态失调的脱发疾病,但其确切发病机制仍不清楚。毛囊(HF)免疫豁免(IP)的崩溃,导致免疫细胞介导的对毛囊的攻击,是目前被广泛接受的AA的基本机制。在这方面研究的免疫细胞中,CD8 T细胞和调节性T(Treg)细胞的研究相对充分,但巨噬细胞在疾病过程中的直接参与较少得到证实。在这篇综述中,我们总结了以往关于巨噬细胞的各种研究,并推测巨噬细胞促成AA发病机制的免疫机制。这一探索为未来的研究和潜在的临床治疗提供了新的见解。

相似文献

1
Macrophage-Centric Immunometabolic Crosstalk in Alopecia Areata Pathogenesis: Mechanisms and Therapeutic Implications.斑秃发病机制中以巨噬细胞为中心的免疫代谢串扰:机制与治疗意义
Clin Rev Allergy Immunol. 2025 May 22;68(1):50. doi: 10.1007/s12016-025-09060-3.
2
Hair follicle immune privilege and its collapse in alopecia areata.毛发滤泡免疫豁免及其在斑秃中的崩溃。
Exp Dermatol. 2020 Aug;29(8):703-725. doi: 10.1111/exd.14155.
3
Collapse and Restoration of Hair Follicle Immune Privilege Ex Vivo: A Model for Alopecia Areata.体外毛囊免疫豁免崩溃与重建:斑秃模型。
Methods Mol Biol. 2020;2154:133-141. doi: 10.1007/978-1-0716-0648-3_11.
4
Hair Follicle Immune Privilege Revisited: The Key to Alopecia Areata Management.重新审视毛囊免疫赦免:斑秃治疗的关键
J Investig Dermatol Symp Proc. 2018 Jan;19(1):S12-S17. doi: 10.1016/j.jisp.2017.10.014.
5
Recent advances in the pathogenesis of autoimmune hair loss disease alopecia areata.自身免疫性脱发疾病斑秃发病机制的最新进展。
Clin Dev Immunol. 2013;2013:348546. doi: 10.1155/2013/348546. Epub 2013 Sep 18.
6
Collapse of immune privilege in alopecia areata: coincidental or substantial?斑秃中免疫特权的崩溃:巧合还是实质?
J Invest Dermatol. 2010 Nov;130(11):2535-7. doi: 10.1038/jid.2010.260.
7
Regulatory T-cells in alopecia areata.斑秃中的调节性T细胞。
J Cutan Pathol. 2019 Sep;46(9):653-658. doi: 10.1111/cup.13479. Epub 2019 May 15.
8
A transcriptomic map of murine and human alopecia areata.鼠和人斑秃的转录组图谱。
JCI Insight. 2020 Jul 9;5(13):137424. doi: 10.1172/jci.insight.137424.
9
Interleukin-15 is a hair follicle immune privilege guardian.白细胞介素-15 是毛囊免疫特权守护者。
J Autoimmun. 2024 May;145:103217. doi: 10.1016/j.jaut.2024.103217. Epub 2024 Apr 5.
10
Deciphering the Complex Immunopathogenesis of Alopecia Areata.解析斑秃的复杂免疫发病机制。
Int J Mol Sci. 2024 May 22;25(11):5652. doi: 10.3390/ijms25115652.

本文引用的文献

1
Metabolic and epigenetic regulation of macrophage polarization in atherosclerosis: Molecular mechanisms and targeted therapies.动脉粥样硬化中巨噬细胞极化的代谢和表观遗传调控:分子机制与靶向治疗
Pharmacol Res. 2025 Feb;212:107588. doi: 10.1016/j.phrs.2025.107588. Epub 2025 Jan 6.
2
Baricitinib inhibits the activation of innate immune cells and exerts therapeutic effects on acute peritonitis and systemic inflammatory response syndrome.巴瑞替尼可抑制先天性免疫细胞的激活,并对急性腹膜炎和全身炎症反应综合征发挥治疗作用。
Int Immunopharmacol. 2024 Dec 25;143(Pt 3):113568. doi: 10.1016/j.intimp.2024.113568. Epub 2024 Nov 2.
3
Macrophage polarization: an important role in inflammatory diseases.
巨噬细胞极化:在炎症性疾病中的重要作用。
Front Immunol. 2024 Apr 10;15:1352946. doi: 10.3389/fimmu.2024.1352946. eCollection 2024.
4
ALKBH5-mediated m6A modification of IL-11 drives macrophage-to-myofibroblast transition and pathological cardiac fibrosis in mice.ALKBH5 介导的 IL-11 的 m6A 修饰驱动小鼠巨噬细胞向肌成纤维细胞转化和病理性心脏纤维化。
Nat Commun. 2024 Mar 5;15(1):1995. doi: 10.1038/s41467-024-46357-x.
5
Metabolic rewiring of macrophages by epidermal-derived lactate promotes sterile inflammation in the murine skin.表皮衍生的乳酸对巨噬细胞的代谢重编程促进了小鼠皮肤的无菌性炎症。
EMBO J. 2024 Apr;43(7):1113-1134. doi: 10.1038/s44318-024-00039-y. Epub 2024 Feb 28.
6
Transcriptome analysis of frontal fibrosis alopecia revealed involvement of immune cells and ferroptosis.额部纤维化性脱发的转录组分析揭示了免疫细胞和铁死亡的参与。
Skin Res Technol. 2024 Feb;30(2):e13608. doi: 10.1111/srt.13608.
7
Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity.人CXCL10的天然羧基末端截短可减弱其与糖胺聚糖的结合、CXCR3A信号传导及淋巴细胞趋化性,同时保留血管生成抑制活性。
Cell Commun Signal. 2024 Feb 2;22(1):94. doi: 10.1186/s12964-023-01453-1.
8
Anti-oxidative, anti-apoptotic, and anti-inflammatory activities of Connarus semidecandrus Jack ethanol extract in UVB-irradiated human keratinocytes.康拉瑞丝半灌木乙醇提取物对 UVB 照射下人角质细胞的抗氧化、抗凋亡和抗炎作用。
J Ethnopharmacol. 2024 Mar 1;321:117574. doi: 10.1016/j.jep.2023.117574. Epub 2023 Dec 13.
9
Inflammatory loops in the epithelial-immune microenvironment of the skin and skin appendages in chronic inflammatory diseases.慢性炎症性疾病中皮肤和皮肤附属器上皮-免疫微环境中的炎症环。
Front Immunol. 2023 Sep 28;14:1274270. doi: 10.3389/fimmu.2023.1274270. eCollection 2023.
10
The potential of regulatory T cell-based therapies for alopecia areata.基于调节性 T 细胞的疗法治疗斑秃的潜力。
Front Immunol. 2023 May 2;14:1111547. doi: 10.3389/fimmu.2023.1111547. eCollection 2023.