Document Detail

S1PR2 links germinal center confinement and growth regulation.
MedLine Citation:
PMID:  22500830     Owner:  NLM     Status:  MEDLINE    
Germinal centers (GCs) are sites of rapid B-cell proliferation and somatic mutation. These ovoid structures develop within the center of follicles and grow to a stereotypic size. The cell migration and interaction dynamics underlying GC B-cell selection events are currently under intense scrutiny. In recent study, we identified a role for a migration inhibitory receptor, S1PR2, in promoting GC B-cell confinement to GCs. S1PR2 also dampens Akt activation and deficiency in S1PR2 or components of its signaling pathway result in a loss of growth control in chronically stimulated mucosal GCs. Herein, we detail present understanding of S1PR2 and S1P biology as it pertains to GC B cells and place this information in the context of a current model of GC function.
Jesse A Green; Jason G Cyster
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Immunological reviews     Volume:  247     ISSN:  1600-065X     ISO Abbreviation:  Immunol. Rev.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-16     Completed Date:  2012-08-10     Revised Date:  2014-09-10    
Medline Journal Info:
Nlm Unique ID:  7702118     Medline TA:  Immunol Rev     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  36-51     Citation Subset:  IM    
Copyright Information:
© 2012 John Wiley & Sons A/S.
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MeSH Terms
B-Lymphocytes / cytology*,  metabolism*
Cell Movement
Gene Deletion
Gene Expression Regulation
Germinal Center / cytology,  immunology,  metabolism*
Oncogene Protein v-akt / genetics,  metabolism
Receptors, Lysosphingolipid / genetics,  metabolism*
Signal Transduction
Grant Support
R01 AI045073/AI/NIAID NIH HHS; R01 AI045073-14/AI/NIAID NIH HHS; R01 AI45073/AI/NIAID NIH HHS; //Howard Hughes Medical Institute; //Howard Hughes Medical Institute
Reg. No./Substance:
0/Receptors, Lysosphingolipid; 0/S1PR2 protein, human; EC Protein v-akt

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