Document Detail

E2-2 regulates the expansion of pro-B cells and follicular versus marginal zone decisions.
MedLine Citation:
PMID:  17082585     Owner:  NLM     Status:  MEDLINE    
The E-proteins E2A, HeLa E-box binding protein, and E2-2 constitute a class of basic helix-loop-helix transcription factors that differentially affect B cell development. E2A is by far the most investigated and appears to operate at several levels during B cell ontogeny. Less is known concerning the role of the other E-proteins. To address the role of E2-2, we have performed transfers of fetal liver (FL) cells into irradiated Rag-deficient mice. Although the transfer of E2-2-deficient cells alone can reconstitute all B cell subpopulations, albeit with a moderate reduction in cellularity, E2-2-deficient cells have a disadvantage when transferred together with wild-type cells. Cultivation of E2-2(-/-) day 14.5 FL cells on stromal cells and IL-7 revealed a reduced frequency of responding B cell progenitors despite normal IL-7Ralpha surface expression. Real-time PCR analysis revealed that E2-2 mRNA expression is high at the pro-B cell stage and drops sharply at the pre-B cell stage, consistent with a role for E2-2 in pro-B cells. In contrast, E2A mRNA was most abundant in pre-B cells. Analysis of the peripheral repertoire revealed that mice reconstituted with E2-2(-/-) FL cells had an increased proportion of marginal zone (MZ) B cells. Interestingly, E2-2 mRNA was elevated approximately 2-fold (p < 0.01) in follicular compared with MZ B cells. Although E2A mRNA showed a similar tendency, the difference was not significant. Collectively, our findings indicate that E2-2 is required for optimal expansion of pro-B cells, and also influences the follicular vs MZ decision.
Ingela Wikström; Johan Forssell; Mario Goncalves; Francesco Colucci; Dan Holmberg
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  177     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-11-03     Completed Date:  2007-01-05     Revised Date:  2009-10-27    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6723-9     Citation Subset:  AIM; IM    
Department of Medical Biosciences, Umeå University, Umeå, Sweden.
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MeSH Terms
B-Lymphocyte Subsets / cytology*,  immunology,  metabolism,  pathology
Cell Differentiation / genetics,  immunology*
Cell Lineage / genetics,  immunology
Cell Proliferation
Cells, Cultured
Interleukin-7 / physiology
Liver / cytology,  embryology,  immunology
Mice, Inbred C57BL
Mice, Knockout
RNA, Messenger / biosynthesis
Spleen / cytology*,  immunology*,  pathology
Stem Cells / cytology*,  immunology,  metabolism,  pathology
TCF Transcription Factors / biosynthesis,  deficiency,  physiology*
Reg. No./Substance:
0/Interleukin-7; 0/RNA, Messenger; 0/TCF Transcription Factors; 0/Tcf7L2 transcription factor

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