CCL18, a chemokine with no known receptor, has been implicated in several fibrotic pulmonary diseases associated with T-lymphocyte infiltration. It has been hypothesized that CCL18 may act through CCR6. Gene delivery of human CCL18 to the lungs of wild-type mice induced pulmonary infiltration of T-lymphocytes, less than 5% of which expressed CCR6. In the lungs of CCR6-deficient mice, CCL18-driven infiltration of T-lymphocytes was attenuated but not fully abrogated. It was concluded that CCR6 is not necessary for CCL18-induced changes in mice in vivo and that CCR6 is not the main functional receptor for CCL18 in this model. © 2012 Luzina and Atamas; licensee BioMed Central Ltd.
CITATION STYLE
Luzina, I. G., & Atamas, S. P. (2012, January 18). CCR6 is not necessary for functional effects of human CCL18 in a mouse model. Fibrogenesis and Tissue Repair. https://doi.org/10.1186/1755-1536-5-2
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