Document Detail

γδT-cell function in sepsis is modulated by C5a receptor signalling.
MedLine Citation:
PMID:  21501163     Owner:  NLM     Status:  MEDLINE    
We previously showed that γδT cells are involved in the pathogenesis of sepsis, but, the underlying mechanisms remained unclear. The present study demonstrates, for the first time, that γδT cells express the complement C5a receptor (C5aR, CD88) and that CD88 expression in γδT cells was up-regulated in mice following sepsis both at protein and mRNA levels. Complement C5a itself contributed to the regulation of C5aR expression on γδT cells, as (i) neutralization of C5a in vivo prevented the expression of C5aR on γδT cells in septic mice and (ii) incubation of mouse spleen cells or purified γδT cells with recombinant C5a in vitro increased CD88 expression by γδT cells at both protein and mRNA levels. C5a receptor on γδT cells also mediates increased interleukin-17 (IL-17) expression as incubation of mouse spleen cells or purified γδT cells with recombinant C5a promotes the IL-17 expression by γδT cells. Ligation of the C5aR on γδT cells activated the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway, which enhances CD88 expression and promotes IL-17 secretion. These results demonstrate that C5a acts directly on the C5aR expressed on γδT cells, resulting in cell activation, and subsequently enhances their capacity for IL-17 production. The up-regulation of the PI3K/Akt pathway following C5a stimulation contributes to up-regulation of γδT-cell function.
Gencheng Han; Shaoxia Geng; Yurong Li; Guojiang Chen; Renxi Wang; Xinying Li; Yuanfang Ma; Beifen Shen; Yan Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-04-19
Journal Detail:
Title:  Immunology     Volume:  133     ISSN:  1365-2567     ISO Abbreviation:  Immunology     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-03     Completed Date:  2011-08-05     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  0374672     Medline TA:  Immunology     Country:  England    
Other Details:
Languages:  eng     Pagination:  340-9     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. Immunology © 2011 Blackwell Publishing Ltd.
Department of Molecular Immunology, Institute of Basic Medical Sciences, Beijing, China.
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MeSH Terms
Cells, Cultured
Complement C5a / immunology*,  pharmacology
Flow Cytometry
Immunologic Factors / pharmacology
Interleukin-17 / metabolism
Mice, Inbred C57BL
Receptor, Anaphylatoxin C5a / genetics,  immunology*
Receptors, Antigen, T-Cell, gamma-delta / immunology*
Recombinant Proteins / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Sepsis / immunology*
Signal Transduction*
T-Lymphocytes / immunology*
Up-Regulation / drug effects
Reg. No./Substance:
0/Immunologic Factors; 0/Interleukin-17; 0/Receptor, Anaphylatoxin C5a; 0/Receptors, Antigen, T-Cell, gamma-delta; 0/Recombinant Proteins; 80295-54-1/Complement C5a

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