Abstract
How the inflammatory response is initiated has been well defined but relatively little is known about how such responses are resolved. Here we show that the D6 chemokine receptor is involved in the post-inflammatory clearance of beta-chemokines from cutaneous sites. After induction of inflammation by phorbol esters, wild-type mice showed a transient inflammatory response. However, in D6-deficient mice, an excess concentration of residual chemokines caused a notable inflammatory pathology with similarities to human psoriasis. These results suggest that D6 is involved in the resolution of the cutaneous inflammatory response.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Chemokine CXCL2
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Chemokine Receptor D6
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Chemokines / immunology
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Chemokines, CC / antagonists & inhibitors
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Chemokines, CC / immunology*
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Chemokines, CC / metabolism
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Dermatitis / immunology*
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Dermatitis / metabolism
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Dermatitis / pathology
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Female
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Histocytochemistry
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Inflammation / immunology
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Inflammation / pathology
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Keratins / immunology
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Mast Cells / immunology
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Mast Cells / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Proliferating Cell Nuclear Antigen / immunology
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Psoriasis / immunology
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Psoriasis / pathology
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Receptors, CCR10
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Receptors, Chemokine / deficiency
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Receptors, Chemokine / immunology*
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Skin / drug effects
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Skin / immunology
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Skin / metabolism
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von Willebrand Factor / immunology
Substances
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Chemokine CXCL2
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Chemokines
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Chemokines, CC
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Cxcl2 protein, mouse
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Proliferating Cell Nuclear Antigen
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Receptors, CCR10
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Receptors, Chemokine
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von Willebrand Factor
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Keratins