Document Detail


IL-21 acts directly on B cells to regulate Bcl-6 expression and germinal center responses.
MedLine Citation:
PMID:  20142429     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During T cell-dependent responses, B cells can either differentiate extrafollicularly into short-lived plasma cells or enter follicles to form germinal centers (GCs). Interactions with T follicular helper (Tfh) cells are required for GC formation and for selection of somatically mutated GC B cells. Interleukin (IL)-21 has been reported to play a role in Tfh cell formation and in B cell growth, survival, and isotype switching. To date, it is unclear whether the effect of IL-21 on GC formation is predominantly a consequence of this cytokine acting directly on the Tfh cells or if IL-21 directly influences GC B cells. We show that IL-21 acts in a B cell-intrinsic fashion to control GC B cell formation. Mixed bone marrow chimeras identified a significant B cell-autonomous effect of IL-21 receptor (R) signaling throughout all stages of the GC response. IL-21 deficiency profoundly impaired affinity maturation and reduced the proportion of IgG1(+) GC B cells but did not affect formation of early memory B cells. IL-21R was required on GC B cells for maximal expression of Bcl-6. In contrast to the requirement for IL-21 in the follicular response to sheep red blood cells, a purely extrafollicular antibody response to Salmonella dominated by IgG2a was intact in the absence of IL-21.
Authors:
Michelle A Linterman; Laura Beaton; Di Yu; Roybel R Ramiscal; Monika Srivastava; Jennifer J Hogan; Naresh K Verma; Mark J Smyth; Robert J Rigby; Carola G Vinuesa
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-08
Journal Detail:
Title:  The Journal of experimental medicine     Volume:  207     ISSN:  1540-9538     ISO Abbreviation:  J. Exp. Med.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-16     Completed Date:  2010-09-20     Revised Date:  2010-09-27    
Medline Journal Info:
Nlm Unique ID:  2985109R     Medline TA:  J Exp Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  353-63     Citation Subset:  IM    
Affiliation:
John Curtin School of Medical Research, Australian National University, Canberra, ACT 2601, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
B-Lymphocytes / immunology*,  metabolism
CD4-Positive T-Lymphocytes / immunology
Cell Communication / immunology
Cell Differentiation / immunology
DNA-Binding Proteins / biosynthesis*,  immunology
Germinal Center / cytology,  immunology*
Immunoglobulin Isotypes / biosynthesis,  genetics
Interleukins / immunology,  metabolism*
Mice
Mice, Inbred C57BL
Receptors, Interleukin-21 / immunology,  metabolism
Sheep
Signal Transduction / immunology
T-Lymphocytes, Helper-Inducer / immunology
Chemical
Reg. No./Substance:
0/Bcl6 protein, mouse; 0/DNA-Binding Proteins; 0/Immunoglobulin Isotypes; 0/Interleukins; 0/Receptors, Interleukin-21; 0/interleukin-21
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