Scholarlink

<p>Pulmonary fibrosis is a category of progressive interstitial lung illnesses caused by atypical inflammatory healing mechanisms, marked by excessive fibroblast activation, aberrant myofibroblast development, and extracellular matrix (ECM) accumulation. Recent research has established that immune cell dysregulation and the aberrant activation of critical signaling pathways are pivotal in the initiation and advancement of fibrosis. Macrophages, neutrophils, dendritic cells, and natural killer (NK) cells collectively constitute a sophisticated innate immune network. M1/M2 polarization, NETs release, and immune surveillance failure are intricately linked to disease development. In adaptive immunity, CD4⁺ T cell subsets facilitate the shift from inflammation to fibrosis via Th1/Th2 imbalance, Th17 amplification, and phase-dependent Treg functionality. B cells aggravate tissue damage through autoantibodies, immunological complexes, and inflammatory cytokines, although regulatory B cells may provide protective effects during certain phases.The TGF-β/Smad signaling pathway is the principal axis of fibrosis, directly governing fibroblast transformation and extracellular matrix deposition. It establishes a highly interconnected signaling network involving pathways including NF-κB, JAK/STAT, and PI3K/AKT, enhancing inflammatory responses and pro-fibrotic effects. The pathogenic etiology of pulmonary fibrosis fundamentally entails immune dysregulation and aberrant tissue repair resulting from interactions between immune cells and signaling pathways. Subsequent investigations ought to amalgamate single-cell omics with spatial transcriptomics to systematically elucidate the spatiotemporal dynamics and essential signaling pathways of immunological subpopulations. This methodology will investigate innovative ways for multi-target combination interventions and microenvironment remodeling, with the objective of establishing theoretical foundations and translational significance for precision medicines in pulmonary fibrosis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The role of immune cell crosstalk and signaling pathways in the pathogenesis of pulmonary fibrosis

  • 期刊论文

  • 发表日期：

    2026年1月19日

查看全文
  • Xia Liu,
  • Haixu Chen,
  • Changying Guo,
  • Yu Lin,
  • Fei Wang,
  • Zhi Lan

摘要

Pulmonary fibrosis is a category of progressive interstitial lung illnesses caused by atypical inflammatory healing mechanisms, marked by excessive fibroblast activation, aberrant myofibroblast development, and extracellular matrix (ECM) accumulation. Recent research has established that immune cell dysregulation and the aberrant activation of critical signaling pathways are pivotal in the initiation and advancement of fibrosis. Macrophages, neutrophils, dendritic cells, and natural killer (NK) cells collectively constitute a sophisticated innate immune network. M1/M2 polarization, NETs release, and immune surveillance failure are intricately linked to disease development. In adaptive immunity, CD4⁺ T cell subsets facilitate the shift from inflammation to fibrosis via Th1/Th2 imbalance, Th17 amplification, and phase-dependent Treg functionality. B cells aggravate tissue damage through autoantibodies, immunological complexes, and inflammatory cytokines, although regulatory B cells may provide protective effects during certain phases.The TGF-β/Smad signaling pathway is the principal axis of fibrosis, directly governing fibroblast transformation and extracellular matrix deposition. It establishes a highly interconnected signaling network involving pathways including NF-κB, JAK/STAT, and PI3K/AKT, enhancing inflammatory responses and pro-fibrotic effects. The pathogenic etiology of pulmonary fibrosis fundamentally entails immune dysregulation and aberrant tissue repair resulting from interactions between immune cells and signaling pathways. Subsequent investigations ought to amalgamate single-cell omics with spatial transcriptomics to systematically elucidate the spatiotemporal dynamics and essential signaling pathways of immunological subpopulations. This methodology will investigate innovative ways for multi-target combination interventions and microenvironment remodeling, with the objective of establishing theoretical foundations and translational significance for precision medicines in pulmonary fibrosis.