NDLI: TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40

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TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40

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TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40

Content Provider	PubMed Central
Author	Jabara, Haifa H. Weng, Yu Sannikova, Tatyana Geha, Raif S.
Copyright Year	2009
Abstract	The isotype switch defect in CD40−/− mice is corrected by wild-type (WT) CD40 transgene, but not by a mutant CD40 transgene that does not bind tumor necrosis factor receptor-associated factors (TRAF) 2 and 3. To define the individual roles of TRAF2 and TRAF3 in CD40 activation of B cells, we introduced mutant CD40 transgenes that selectively lack the ability to bind TRAF2 (ΔTR2), TRAF3 (ΔTR3) or both (ΔTR2,3) into B cells of CD40−/− mice. Serum IgG1 and IgE levels, IgG1 antibody response to sub-optimal doses of the T cell-dependent antigen keyhole limpet hemocyanin, germinal center formation, CD40-mediated proliferation, isotype switching and activation of the non-canonical NF-κB pathway were partially diminished in ΔTR2 and ΔTR3 mice and virtually absent in ΔTR2,3 mice. These results suggest that TRAF2 and TRAF3 can each independently mediate class switch recombination (CSR) driven by CD40, but both are required for optimal CD40-driven isotype switching.
Related Links	http://dx.doi.org/10.1093/intimm/dxp013
Ending Page	488
Page Count	12
Starting Page	477
File Format	PDF
ISSN	09538178
e-ISSN	14602377
Journal	International Immunology
Issue Number	4
Volume Number	21
Language	English
Publisher	Oxford University Press
Publisher Date	2009-04-01
Access Restriction	Open
Rights Holder	Oxford University Press
Subject Keyword	Immunology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40

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TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40

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TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40

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TRAF2 and TRAF3 independently mediate Ig class switching driven by CD40