Abstract

CD4 ⁺ T cells direct immune responses against infectious microorganisms but are also involved in the pathogenesis of inflammatory diseases. In the last two to three decades, various researchers have identified and characterized several functional CD4 ⁺ T cell subsets, including T-helper 1 (Th1), Th2, Th9 and Th17 cells and regulatory T (Treg) cells. In this mini-review, we introduce the concept of pathogenic Th cells that induce inflammatory diseases with a model of disease induction by a population of pathogenic Th cells; “pathogenic Th population disease-induction model”. We will focus on Th2 cells that induce allergic airway inflammation—pathogenic Th2 cells (Tpath2 cells)—and discuss the nature of Tpath2 cells that shape the pathology of chronic inflammatory diseases. Various Tpath2 cell subsets have been identified and their unique features are summarized in mouse and human systems. Second, we will discuss how Th cells migrate and are maintained in chronic inflammatory lesions. We propose a model known as the “CD69–Myl9 system”. CD69 is a cell surface molecule expressed on activated T cells and interaction with its ligand myosin light chain 9 (Myl9) is required for the induction of inflammatory diseases. Myl9 molecules in the small vessels of inflamed lungs may play a crucial role in the migration of activated T cells into inflammatory lesions. Emerging evidence may provide new insight into the pathogenesis of chronic inflammatory diseases and contribute to the development of new therapeutic strategies for intractable inflammatory disorders.

中文翻译：

---

炎症性疾病中的 CD4 + T 细胞：致病性 T 辅助细胞和 CD69–Myl9 系统

摘要

CD4 ⁺ T 细胞直接针对感染性微生物的免疫反应，但也参与炎症性疾病的发病机制。在过去的两到三十年中，各种研究人员已经确定并表征了几种功能性 CD4 ⁺T 细胞亚群，包括 T 辅助细胞 1 (Th1)、Th2、Th9 和 Th17 细胞以及调节性 T (Treg) 细胞。在这篇小型综述中，我们介绍了诱发炎症性疾病的致病性 Th 细胞的概念，以及由一组致病性 Th 细胞引起的疾病诱导模型。“致病性Th人群疾病诱导模型”。我们将重点关注诱导过敏性气道炎症的 Th2 细胞——致病性 Th2 细胞（Tpath2 细胞）——并讨论影响慢性炎症性疾病病理学的 Tpath2 细胞的性质。已经鉴定了各种 Tpath2 细胞亚群，并在小鼠和人类系统中总结了它们的独特特征。其次，我们将讨论 Th 细胞如何在慢性炎症病变中迁移和维持。我们提出了一种称为“CD69-Myl9 系统”的模型。CD69 是一种在活化的 T 细胞上表达的细胞表面分子，它与配体肌球蛋白轻链 9 (Myl9) 的相互作用是诱导炎症性疾病所必需的。发炎的肺小血管中的 Myl9 分子可能在活化的 T 细胞迁移到炎症病变中起关键作用。新出现的证据可能为慢性炎症性疾病的发病机制提供新的见解，并有助于开发针对难治性炎症性疾病的新治疗策略。