增生异常上皮修复促进淋巴细胞的组织驻留，抑制病毒感染后肺泡再生，这一成果由上海科技大学席莹研究组经过不懈努力而取得。该研究于2025年12月23日发表于国际一流学术期刊《细胞—干细胞》杂志上。

研究人员发现，在严重病毒感染后出现的发育不良的KRT5⁺基底样细胞，在病毒清除后以依赖CXCR3-和整合素α4β7的方式参与肺中CD4⁺效应细胞和CD8⁺ T细胞的募集和隔离。持久性CD4⁺效应细胞和CD8⁺ T细胞通过分泌IFNγ损害气道分泌细胞介导的肺泡再生，从而抑制肺功能修复。重要的是，抗ifn - γ治疗可改善体内肺泡再生和肺功能。总的来说，他们的研究揭示了发育不良的KRT5⁺细胞在肺泡再生中的发病作用，作为组织驻留淋巴细胞特异性抑制肺泡再生的生态位。此外，他们的发现为改善病毒性肺炎后肺泡再生提供了一种潜在的治疗策略。

据介绍，严重的呼吸道病毒感染会导致肺泡上皮的广泛损伤，并引起免疫反应。免疫微环境如何与肺干/祖细胞相互作用并影响肺泡再生尚不清楚。

附：英文原文

Title: Dysplastic epithelial repair promotes the tissue residence of lymphocytes to inhibit alveolar regeneration post viral infection

Author: Tiantian Lu, Li Liu, Ping Wang, Zhe Chen, Pei Wu, Jiawei Chen, Guilin Peng, Ruijuan Guan, Chaoqun Wang, Pengfei Sui, Haopeng Wang, Xiao Su, Jincun Zhao, Tao Ren, Ying Xi

Issue&Volume: 2025-12-23

Abstract: Severe respiratory viral infections lead to extensive damage to the alveolar epithelium and also induce a robust immune response. How the immune microenvironment interacts with lung stem/progenitor cells and impacts alveolar regeneration is poorly understood. Here, we found that dysplastic KRT5+ basal-like cells, which emerge after severe viral infections, contribute to the recruitment and sequestration of CD4+ effector and CD8+ T cells in the lung after viral clearance in a CXCR3- and integrin α4β7-dependent manner. Persistent CD4+ effector and CD8+ T cells impair alveolar regeneration mediated via airway secretory cells by secreting IFNγ, thereby inhibiting lung functional repair. Importantly, anti-IFNγ treatment improves alveolar regeneration and lung function in vivo. Overall, our study reveals the pathogenetic role of dysplastic KRT5+ cells in alveolar regeneration, serving as a niche for tissue-resident lymphocytes that specifically inhibit alveolar regeneration. Additionally, our findings provide a potential therapeutic strategy to improve alveolar regeneration after viral pneumonia.

DOI: 10.1016/j.stem.2025.12.005

Source: https://www.cell.com/cell-stem-cell/abstract/S1934-5909(25)00439-4