Frontiers in immunology · 2026
CCL20-CCR6 axis mediates mucosal-associated invariant T-M2 macrophage crosstalk to drive immune dysregulation in liver cirrhosis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen Bochen, Li Ruoling, Zhang Shuya, Lou Yiting, Zhang Shuo, Lou Jiaheng, Zhang Jingcheng, Xu Chuyun, Jiang Tao, Lv Yuanlin
Аннотация
INTRODUCTION: Cirrhosis is the end-stage of chronic liver disease characterized by progressive hepatic fibrosis and persistent immune dysregulation, yet the mechanisms by which immune cell crosstalk drives disease progression remain poorly understood.
METHODS: In the present study, we integrated bulk and single-cell transcriptomic analyses with immunofluorescence validation to investigate the role of the CCL20-CCR6 axis in MAIT cells-macrophages interactions during cirrhosis progression.
RESULTS: We identified eight core cirrhosis-associated immune genes (OGN, IL32, CCL19, PDGFA, CCL20, NTS, SEMA3C, HSPA2), among which CCL20 was selectively enriched in mucosal-associated invariant T cells (MAIT) and closely associated with their activation- and exhaustion-related transcriptional profiles. Cell-cell communication analysis revealed that the CCL20-CCR6 axis may specifically mediate bidirectional interactions between MAIT cells and M2 macrophages, forming a disease-specific positive feedback loop within the cirrhotic microenvironment. Immunofluorescence staining further confirmed the enrichment and colocalization of CCL20, MAIT cells, and M2 macrophages in cirrhotic tissues.
DISCUSSION: Collectively, these findings support the CCL20-CCR6 axis as a key regulator of hepatic immune dysregulation and fibrotic progression in liver cirrhosis, highlighting its potential as both a biomarker of disease activity and a therapeutic target for cirrhosis intervention.
METHODS: In the present study, we integrated bulk and single-cell transcriptomic analyses with immunofluorescence validation to investigate the role of the CCL20-CCR6 axis in MAIT cells-macrophages interactions during cirrhosis progression.
RESULTS: We identified eight core cirrhosis-associated immune genes (OGN, IL32, CCL19, PDGFA, CCL20, NTS, SEMA3C, HSPA2), among which CCL20 was selectively enriched in mucosal-associated invariant T cells (MAIT) and closely associated with their activation- and exhaustion-related transcriptional profiles. Cell-cell communication analysis revealed that the CCL20-CCR6 axis may specifically mediate bidirectional interactions between MAIT cells and M2 macrophages, forming a disease-specific positive feedback loop within the cirrhotic microenvironment. Immunofluorescence staining further confirmed the enrichment and colocalization of CCL20, MAIT cells, and M2 macrophages in cirrhotic tissues.
DISCUSSION: Collectively, these findings support the CCL20-CCR6 axis as a key regulator of hepatic immune dysregulation and fibrotic progression in liver cirrhosis, highlighting its potential as both a biomarker of disease activity and a therapeutic target for cirrhosis intervention.