Document Detail


Immature dendritic cells reduce proinflammatory cytokine production by a coculture of macrophages and apoptotic cells in a cell-to-cell contact-dependent manner.
MedLine Citation:
PMID:  14761936     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have demonstrated that phagocytosis of late apoptotic cells by mouse macrophages leads to the production of proinflammatory cytokines, notably macrophage-inflammatory protein (MIP-2), and therefore, a yet-unknown mechanism(s) should keep our body free of inflammation. In this study, we examined the effect of the addition of immature dendritic cells (iDCs) to a coculture of macrophages and apoptotic cells on MIP-2 production and phagocytosis by macrophages. The addition of iDCs to the coculture reduced MIP-2 production significantly but unexpectedly enhanced the phagocytosis by macrophages. Further study revealed that the reduction of MIP-2 production was dependent on cell-to-cell contact partly involving the beta(2) integrin family Mac-1. In addition, anti-inflammatory cytokines, interleukin-10 and transforming growth factor-beta, were involved in the reduction of MIP-2 production, as antibodies against these cytokines recovered MIP-2 production. Both cytokines were expressed by iDCs more significantly than macrophages at the mRNA levels, although they were hardly detected in the supernatant at the protein levels, suggesting that minute amounts of these anti-inflammatory cytokines were produced mainly by iDCs to block MIP-2 production in a cell-to-cell contact-dependent manner. Thus, this study reveals a new mechanism by which MIP-2 production by macrophages phagocytosing apoptotic cells is prevented.
Authors:
Munehisa Takahashi; Kahori Kurosaka; Yoshiro Kobayashi
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Publication Detail:
Type:  Journal Article     Date:  2004-02-03
Journal Detail:
Title:  Journal of leukocyte biology     Volume:  75     ISSN:  0741-5400     ISO Abbreviation:  J. Leukoc. Biol.     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-05-03     Completed Date:  2004-06-11     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8405628     Medline TA:  J Leukoc Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  865-73     Citation Subset:  IM    
Affiliation:
Department of Biomolecular Science, Faculty of Science, Toho University, Chiba, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / immunology*
Cell Communication / immunology*
Cells, Cultured
Chemokine CXCL2
Coculture Techniques
Cytokines / biosynthesis*,  pharmacology
Dendritic Cells / cytology,  immunology*
Down-Regulation / immunology
Inflammation / immunology
Interleukin-10 / pharmacology
Interleukin-6 / biosynthesis
Macrophages / cytology*,  immunology
Male
Mice
Mice, Inbred C57BL
Monokines / biosynthesis
T-Lymphocytes
Transforming Growth Factor beta / pharmacology
Chemical
Reg. No./Substance:
0/Chemokine CXCL2; 0/Cytokines; 0/Interleukin-6; 0/Monokines; 0/Transforming Growth Factor beta; 130068-27-8/Interleukin-10

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