Abstract:
:To define the role of TRAF proteins in CD40-dependent isotype switching in B cells, we introduced wild-type (WT) and mutant CD40 transgenes that lacked the binding motifs for TRAF6 (CD40deltaTRAF6), TRAF2 and TRAF3 (CD40deltaTRAF2/3), or both (CD40deltaTRAFs) into B cells of CD40(-/-) mice. The in vivo isotype switch defect in CD40(-/-) mice was fully corrected by WT and CD40deltaTRAF6, partially by CD40deltaTRAF2/3, and not at all by CD40deltaTRAFs transgenes. CD40-mediated isotype switching, proliferation, and activation of p38, JNK, and NFkappaB in B cells were normal in WT and CD40deltaTRAF6 mice, severely impaired in CD40deltaTRAF2/3, and absent in CD40deltaTRAFs mice. These results suggest that binding to TRAF2 and/or TRAF3 but not TRAF6 is essential for CD40 isotype switching and activation in B cells.
journal_name
Immunityjournal_title
Immunityauthors
Jabara H,Laouini D,Tsitsikov E,Mizoguchi E,Bhan A,Castigli E,Dedeoglu F,Pivniouk V,Brodeur S,Geha Rdoi
10.1016/s1074-7613(02)00394-1keywords:
subject
Has Abstractpub_date
2002-09-01 00:00:00pages
265-76issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(02)00394-1journal_volume
17pub_type
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