Warning: The NCBI web site requires JavaScript to function. more...
Generate a file for use with external citation management software.
Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA. satamas@umaryland.edu.
ABSTRACT: 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.
Images from this publication.See all images (1) Free text
Your browsing activity is empty.
Activity recording is turned off.
Turn recording back on