Abstract：
Chronic Lung Allograft Dysfunction (CLAD) is a critical post-transplant complication that predominantly determines the long-term survival rates and quality of life of patients undergoing lung transplantation. The limited efficacy of current immunosuppressive strategies underscores our incomplete understanding of the immunological aspects of CLAD. Hence, there is an urgent need for more comprehensive and targeted research to unravel the complex interplay of immune cells in the development and progression of CLAD. This study conducts an in-depth analysis of the immune environment in CLAD. By examining the gene expression profiles of T cells, natural killer cells, B cells, macrophages, and monocytes, we have elucidated a unique immunological landscape in CLAD compared to healthy controls. We highlight the heterogeneity within the immune populations and provide a comprehensive understanding of the immune mechanisms driving CLAD. Enrichment analysis identified specific pathways that are either overactive or suppressed in CLAD, revealing potential molecular targets for therapeutic intervention. Our findings emphasize the crucial role of T cells in the pathophysiology of CLAD, coordinating the immune response and revealing an amplified immune cell network, potentially leading to maladaptive tissue responses. By integrating a comprehensive cellular and molecular portrait of the immune environment, our research not only deepens our understanding of the pathogenesis of CLAD but also lays a foundational approach for the development of targeted therapies.
摘要：
慢性同种异体肺移植功能障碍（CLAD）是一种严重的移植后并发症，主要决定了接受肺移植的患者的长期生存率和生活质量。当前免疫抑制策略的有限功效强调了我们对CLAD的免疫学方面的不完全理解。因此，迫切需要更全面和有针对性的研究，以揭示免疫细胞在CLAD发生和发展过程中的复杂相互作用。本研究对CLAD的免疫环境进行了深入分析。通过检测T细胞的基因表达谱,自然杀伤细胞,B细胞,巨噬细胞，和单核细胞，与健康对照相比，我们已经阐明了CLAD的独特免疫学景观。我们强调了免疫群体内的异质性，并全面了解了驱动CLAD的免疫机制。富集分析确定了CLAD中过度活跃或抑制的特定途径，揭示治疗干预的潜在分子靶标。我们的发现强调了T细胞在CLAD病理生理学中的关键作用。协调免疫反应并揭示放大的免疫细胞网络，可能导致适应不良的组织反应。通过整合免疫环境的全面细胞和分子肖像，我们的研究不仅加深了我们对CLAD发病机制的理解,而且为靶向治疗的发展奠定了基础.
