Document Detail

The induction of inflammation by dectin-1 in vivo is dependent on myeloid cell programming and the progression of phagocytosis.
MedLine Citation:
PMID:  18714028     Owner:  NLM     Status:  MEDLINE    
Dectin-1 is the archetypal signaling, non-Toll-like pattern recognition receptor that plays a protective role in immune defense to Candida albicans as the major leukocyte receptor for beta-glucans. Dectin-1-deficiency is associated with impaired recruitment of inflammatory leukocytes and inflammatory mediator production at the site of infection. In this study, we have used mice to define the mechanisms that regulate the dectin-1-mediated inflammatory responses. Myeloid cell activation by dectin-1 is controlled by inherent cellular programming, with distinct macrophage and dendritic cell populations responding differentially to the engagement of this receptor. The inflammatory response is further modulated by the progression of the phagocytosis, with "frustrated phagocytosis" resulting in dramatically augmented inflammatory responses. These studies demonstrate that dectin-1 in isolation is sufficient to drive a potent inflammatory response in a context-dependent manner. This has implications for the mechanism by which myeloid cells are activated during fungal infections and the processes involved in the therapeutic manipulation of the immune system via exogenous dectin-1 stimulation or blockade.
Marcela Rosas; Kate Liddiard; Matti Kimberg; Inês Faro-Trindade; Jacqueline U McDonald; David L Williams; Gordon D Brown; Philip R Taylor
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  181     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2008 Sep 
Date Detail:
Created Date:  2008-08-20     Completed Date:  2008-09-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3549-57     Citation Subset:  AIM; IM    
Medical Biochemistry and Immunology, Cardiff University School of Medicine, Cardiff, United Kingdom.
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MeSH Terms
Candida albicans / immunology
Dendritic Cells
Inflammation / etiology*
Membrane Proteins / deficiency,  physiology*
Mice, Knockout
Mycoses / immunology
Myeloid Cells / physiology*
Nerve Tissue Proteins / deficiency,  physiology*
beta-Glucans / immunology
Grant Support
53522//PHS HHS; G0601617//Medical Research Council; //Wellcome Trust
Reg. No./Substance:
0/Membrane Proteins; 0/Nerve Tissue Proteins; 0/beta-Glucans; 0/dectin 1

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