中国麻风皮肤病杂志 ›› 2026, Vol. 42 ›› Issue (7): 536-541.doi: 10.12144/zgmfskin202607536

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CARD11突变与调节性T细胞功能失调在特应性皮炎中的研究进展

高明萱,吴娟,汪旸,赵嘉惠   

  1. 北京大学第一医院皮肤性病科，皮肤病与性病国家临床医学研究中心，北京，100034
  • 出版日期:2026-07-15 发布日期:2026-06-29

Research progress on CARD11 mutations and regulatory T cell dysfunction in atopic dermatitis

GAO Mingxuan, WU Juan, WANG Yang, ZHAO Jiahui   

  1. Department of Dermatology and Venereology, Peking University First Hospital, National Clinical Research Center for Skin and Sexually Transmitted Diseases, Beijing 100034, China
  • Online:2026-07-15 Published:2026-06-29

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摘要： 特应性皮炎（atopic dermatitis,AD）是一种常见的慢性炎症性皮肤病，其发病机制与遗传和免疫紊乱密切相关。CARD11作为CBM信号复合体的核心成员，是淋巴细胞抗原受体信号传导的关键中介。近期研究发现，CARD11的多种突变类型可干扰调节性T细胞（Treg）的发育与功能，导致免疫耐受失衡，进而驱动AD的发生与发展。本文综述了CARD11的生物学基础、突变相关疾病及其调控Treg功能的分子机制，为AD的精准免疫治疗提供理论参考。

关键词: CARD11, 特应性皮炎, 调节性T细胞, 信号传导

Abstract: Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with genetic susceptibility and immune dysregulation. CARD11, a scaffolding protein in the CARD11-BCL10-MALT1 (CBM) complex, plays a central role in lymphocyte antigen receptor signaling. Recent studies have identified that various CARD11 mutations disrupt the development and function of regulatory T cells (Tregs), leading to a breakdown in immune tolerance that drives AD. This review summarizes the biological basis of CARD11, the clinical syndromes associated with its mutations, and the specific mechanisms of Treg dysfunction in AD, providing insights for targeted therapeutic strategies.

Key words: CARD11, atopic dermatitis, regulatory T cells, signal transduction