NDLI: Cell-autonomous regulation of neutrophil migration by the D6 chemokine decoy receptor.

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Cell-autonomous regulation of neutrophil migration by the D6 chemokine decoy receptor.

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What is and what should always have been: long-lived plasma cells induced by T cell-independent antigens.

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Cell-autonomous regulation of neutrophil migration by the D6 chemokine decoy receptor.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Pruenster, Monika Nibbs, Robert J. B. Jamieson, Thomas Graham, Gerard J. Rot, Antal McKimmie, Clive Burt, Claire L. Pallas, Kenneth J. Horuk, Richard
Description	Country affiliation: Austria Author Affiliation: Rot A ( Novartis Institutes for BioMedical Research, Vienna A1235, Austria.)
Abstract	Chemokines, acting on their cognate receptors on infiltrating leukocytes, drive the inflammatory response. We have been interested in determining roles and potential mechanisms for the atypical chemokine-scavenging receptor D6 in the regulation of inflammation. In this study, we show that a psoriasis-like pathology that arises in inflamed skins of D6-deficient mice is characterized by a massive and aberrant localization of neutrophils to the dermal/epidermal junction, which is associated with development of the pathology. Such misplacement of neutrophils is also seen with D6-deficient mice in other inflammatory models, suggesting a role for D6 in the spatial positioning of neutrophils within inflamed sites. We further show that D6 functions cell autonomously in this context and that D6, expressed by neutrophils, limits their migrational responses to CCR1 ligands such as CCL3. Our data therefore indicate that D6 is able to play a cell-autonomous role as a migratory rheostat restricting migration of D6-expressing cells such as neutrophils toward ligands for coexpressed inflammatory chemokine receptors. These data have important implications for our understanding of the roles for D6 in regulating inflammation and for our understanding of the control of spatial positioning of leukocytes at inflamed sites.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201429
Journal	The Journal of Immunology
Issue Number	12
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Immune System Diseases Immunology Leukocyte Disorders Psoriasis Receptors, Chemokine Animals Disease Models, Animal Inflammation Mice Mice, Knockout Microscopy, Confocal Pathology Skin Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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