Document Detail


Intrinsic Toll-like receptor signalling drives regulatory function in B cells.
MedLine Citation:
PMID:  23276971     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
B cells can contribute to immunity through production of antibodies, presentation of antigen to T cells, and secretion of cytokines. B cell activation can result in various outcomes for the host. In general B cell responses are beneficial during infections, and deleterious during autoimmune diseases. However, B cells can also limit host defence against pathogens, and protect from autoimmune pathologies. B cells can therefore act both as drivers and as regulators of immunity. Understanding how these opposite functions are mediated shall stimulate the elaboration of novel approaches for manipulating the immune system. B cells might acquire distinct functional properties depending on their mode of activation. Antigen-specific B cell responses require triggering of B cell receptor (BCR) by antigen, and provision of helper signals by T cells. B cells also express various innate immune receptors, and can directly respond to microbial products. Here, we discuss how intrinsic signalling via Toll-like receptors contributes to the suppressive functions of B cells during autoimmune and infectious diseases.
Authors:
Ping Shen; Vicky Lampropoulou; Ulrik Stervbo; Ellen Hilgenberg; Stefanie Ries; Aurelie Mecqinion; Simon Fillatreau
Publication Detail:
Type:  Journal Article     Date:  2013-01-01
Journal Detail:
Title:  Frontiers in bioscience (Elite edition)     Volume:  5     ISSN:  1945-0508     ISO Abbreviation:  Front Biosci (Elite Ed)     Publication Date:  2013  
Date Detail:
Created Date:  2013-01-01     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101485240     Medline TA:  Front Biosci (Elite Ed)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  78-86     Citation Subset:  IM    
Affiliation:
Immune regulation group, Deutsche Rheuma-Forschungszentrum, a Leibniz institute, Chariteplatz 1, 10117 Berlin, Germany.
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