Table 1 Summary table of CCL20-CCR6 in the respiratory system
From: Correction: Progress of CCL20-CCR6 in the airways: a promising new therapeutic target
Name | frequency | Action mechanism | Effector cell | Phenotype | Reference |
|---|---|---|---|---|---|
Asthma | ↑ | The secretion of CCL20 by airway epithelium is stimulated by MAPK and AKT pathways under the stimulation of related inflammatory factors. | DCs, Treg | Harmful | [65], [67] |
NSCLC | ↑ | NSCLC cells promote CCL20 production and induce lung cancer cell migration through MAPK, Wnt, and PI3K pathways. | Th17, Treg, ILC3s | Harmful | [76] |
COPD | ↑ | Activation and activation of TGF-β induced by integrin avβ8 enhances CCL20 transcription and exacerbates airway fibrosis. | DCs | Harmful | [92–93] |
Pulmonary tuberculosis | ↑ | Induces T lymphocytes to migrate to the site of inflammation. | CD4+ T, CD8+T | Harmful | [99] |
Pulmonary nodular disease | ↑ | Stimulate the activation of the PI3k/Akt pathway, causing Th17/Treg imbalance; Activate the TGF-β/Smad pathway. | Treg, Th1, Th17 | Harmful | [107–108] |
Pulmonary aspergillosis | ↓ | By depleting CCL20, the innate immune response of the host is suppressed. | Th1, Th2, Th17 | Protective | [113] |
Viral Infectious Pneumonia | ↑ | The imbalance of Th17/Treg cells and the decreased ability of CD8+T cells to clear the virus aggravate lung inflammation. | Treg, Th17 | Harmful | [116] |