Document Detail


Hepatic B cells are readily activated by Toll-like receptor-4 ligation and secrete less interleukin-10 than lymphoid tissue B cells.
MedLine Citation:
PMID:  23617623     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
B cells perform various immunological functions that include production of antibody, presentation of antigens, secretion of multiple cytokines and regulation of immune responses mainly via their secretion of interleukin (IL)-10. While the liver is regarded both as an important immune organ and a tolerogenic environment, little is known about the functional biology of hepatic B cells. In this study we demonstrate that, following lipopolysaccharide (LPS) stimulation in vivo, normal mouse hepatic B cells rapidly increase their surface expression of CD39, CD40, CD80 and CD86, and produce significantly elevated levels of proinflammatory interferon (IFN)-γ, IL-6 and tumour necrosis factor (TNF)-α compared with splenic B cells. Moreover, LPS-activated hepatic B cells produce very low levels of IL-10 compared with activated splenic B cells that produce comparatively high levels of this immunosuppressive cytokine. Splenic, but not hepatic, B cells inhibited the activation of liver conventional myeloid dendritic cells (mDCs). Furthermore, compared with the spleen, the liver exhibited significantly smaller proportions of B1a and marginal zone-like B cells, which have been shown to produce IL-10 upon LPS stimulation. These data suggest that, unlike in the spleen, IL-10-producing regulatory B cells in the liver are not a prominent cell type. Consistent with this, when compared with liver conventional mDCs from B cell-deficient mice, those from B cell-competent wild-type mice displayed enhanced expression of the cell surface co-stimulatory molecule CD86, greater production of proinflammatory cytokines (IFN-γ, IL-6, IL-12p40) and reduced secretion of IL-10. These findings suggest that hepatic B cells have the potential to initiate rather than regulate inflammatory responses.
Authors:
H Zhang; D B Stolz; G Chalasani; A W Thomson
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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:  Clinical and experimental immunology     Volume:  173     ISSN:  1365-2249     ISO Abbreviation:  Clin. Exp. Immunol.     Publication Date:  2013 Sep 
Date Detail:
Created Date:  2013-08-07     Completed Date:  2013-10-22     Revised Date:  2014-03-24    
Medline Journal Info:
Nlm Unique ID:  0057202     Medline TA:  Clin Exp Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  473-9     Citation Subset:  IM    
Copyright Information:
© 2013 British Society for Immunology.
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MeSH Terms
Descriptor/Qualifier:
Animals
B-Lymphocytes / immunology*,  metabolism*
Dendritic Cells / immunology,  metabolism
Interferon-gamma / biosynthesis
Interleukin-10 / biosynthesis*
Lipopolysaccharides / immunology
Liver / immunology*,  metabolism
Lymphoid Tissue / immunology*,  metabolism
Male
Mice
Toll-Like Receptor 4 / metabolism*
Tumor Necrosis Factor-alpha / biosynthesis
Grant Support
ID/Acronym/Agency:
P01 AI081678/AI/NIAID NIH HHS; P01AI81678/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Lipopolysaccharides; 0/Toll-Like Receptor 4; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10; 82115-62-6/Interferon-gamma

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