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Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Immunol 2014 ; 193 (11): 5515-24 Nephropedia Template TP
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Deleted in Breast Cancer 1 (DBC1) is a Suppressor of B cell Activation by Negatively Regulating Alternative NF-?B Transcriptional Activity #MMPMID25362179
Kong S; Thiruppathi M; Qiu Q; Lin Z; Dong H; Chini EN; Prabhakar BS; Fang. D
J Immunol 2014[Dec]; 193 (11): 5515-24 PMID25362179show ga
CD40 and BAFF receptor (BAFFR) signaling plays important roles in B cell proliferation and immunoglobulin production. In this study we found that B cells from mice with deletion of Dbc1 gene (Dbc1?/?) show elevated proliferation, and IgG1 and IgA production upon in vitro CD40 and BAFF, but not BCR and LPS stimulation, indicating that DBC1 inhibits CD40/BAFF-mediated B cell activation in a cell-intrinsic manner. Microarray analysis and Chromatin Immunoprecipitation (ChIP) experiments reveal that DBC1 inhibits B cell function by selectively suppressing the transcriptional activity of alternative NF-?B members RelB and p52 upon CD40 stimulation. As a result, when immunized with Nitrophenylated-Keyhole Limpet Hemocyanin (NP-KLH), Dbc1?/? mice produce significantly increased levels of germinal center B cells, plasma cells, as well as antigen-specific immunoglobulin. Finally, loss of DBC1 in mice leads to higher susceptibility to Experimental Autoimmune Myasthenia Gravis (EAMG). Our study identifies DBC1 as a novel regulator of B cell activation by suppressing the alternative NF-?B pathway.