Differential Signaling via Tumor Necrosis Factor-Associated Factors (TRAFs) by CD27 and CD40 in Mouse B Cells.
- Author:
So Youn WOO
1
;
Hae Kyung PARK
;
Gail A BISHOP
Author Information
- Publication Type:Original Article
- Keywords: B cell; CD40; CD27; TRAF2; TRAF3
- MeSH: Animals; B-Lymphocytes*; Cell Line; Humans; Immunoglobulin M; Killer Cells, Natural; Ligation; Membranes; Memory; Mice*; Necrosis*; Receptors, Tumor Necrosis Factor; T-Lymphocytes; TNF Receptor-Associated Factor 2; TNF Receptor-Associated Factor 3; TNF Receptor-Associated Factor 5; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
- From:Immune Network 2004;4(3):143-154
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: CD27 is recently known as a memory B cell marker and is mainly expressed in activated T cells, some B cell population and NK cells. CD27 is a member of tumor necrosis factor receptor family. Like CD40 molecule, CD27 has (P/S/T/A) X(Q/E)E motif for interacting with TNF receptor-associated factors (TRAFs), and TRAF2 and TRAF5 bindings to CD27 in 293T cells were reported. METHODS: To investigate the CD27 signaling effect in B cells, human CD40 extracellular domain containing mouse CD27 cytoplamic domain construct (hCD40-mCD27) was transfected into mouse B cell line CH12.LX and M12.4.1. RESULTS: Through the stimulation of hCD40-mCD27 molecule via anti-human CD40 antibody or CD154 ligation, expression of CD11a, CD23, CD54, CD70 and CD80 were increased and secretion of IgM was induced, which were comparable to the effect of CD40 stimulation. TRAF2 and TRAF3 were recruited into lipid-enriched membrane raft and were bound to CD27 in M12.4.1 cells. CD27 stimulation, however, did not increase TRAF2 or TRAF3 degradation. CONCLUSION: In contrast to CD40 signaling pathway, TRAF2 and TRAF3 degradation was not observed after CD27 stimulation and it might contribute to prolonged B cell activation through CD27 signaling.
