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    Fibrogenesis Tissue Repair. 2012 Jan 18;5(1):2.

    CCR6 is not necessary for functional effects of human CCL18 in a mouse model.

    Source

    Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA. satamas@umaryland.edu.

    Abstract

    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.

    PMID:
    22257697
    [PubMed - in process]
    PMCID:
    PMC3274466
    Free PMC Article

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