Progress of CCL20-CCR6 in the airways: a promising new therapeutic target

Journal of Inflammation

Table 1 Summary table of CCL20-CCR6 in the respiratory system

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	[5, 65]
NSCLC	↑	NSCLC cells promote CCL20 production and induce lung cancer cell migration through MAPK, Wnt, and PI3K pathways.	Th17, Treg, ILC3s	Harmful	[73]
COPD	↑	Activation and activation of TGF-β induced by integrin avβ8 enhances CCL20 transcription and exacerbates airway fibrosis.	DCs	Harmful	[88, 89]
Pulmonary tuberculosis	↑	Induces T lymphocytes to migrate to the site of inflammation.	CD4⁺ T, CD8⁺T	Harmful	[95]
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	[103, 104]
Pulmonary aspergillosis	↓	By depleting CCL20, the innate immune response of the host is suppressed.	Th1, Th2, Th17	Protective	[109]
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	[112]

The ↑ symbol indicates an increase in expression levels, the ↓symbol indicates a decrease in expression levels

ISSN: 1476-9255