Journal
FIBROGENESIS & TISSUE REPAIR
Volume 5, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1755-1536-5-2
Keywords
CCL18; CCR6; fibrosis; inflammation; T-lymphocytes
Categories
Funding
- VA Merit Awards
- NIHNHLBI [1R21HL106196]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R21HL106196] Funding Source: NIH RePORTER
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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.
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