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TNF receptor-associated factor 3 restrains B-cell receptor signaling in normal and malignant B cells
Journal article   Open access   Peer reviewed

TNF receptor-associated factor 3 restrains B-cell receptor signaling in normal and malignant B cells

Amy L. Whillock, Tiffany K. Ybarra and Gail A. Bishop
The Journal of biological chemistry, Vol.296, pp.100465-100465
01/2021
DOI: 10.1016/j.jbc.2021.100465
PMCID: PMC8042179
PMID: 33639170
url
https://doi.org/10.1016/j.jbc.2021.100465View
Published (Version of record) Open Access

Abstract

TRAF3 has diverse signaling functions, which vary by cell type. Uniquely in B lymphocytes, TRAF3 inhibits homeostatic survival. Highlighting the role of TRAF3 as a tumor suppressor, loss-of-function TRAF3 mutations are associated with human B-cell malignancies, while B-cell-specific deletion of TRAF3 in mice leads to autoimmunity and lymphoma development. The role of TRAF3 in inhibiting noncanonical NF-κB activation, CD40 and BAFF-R signaling to B cells is well documented. In contrast, TRAF3 enhances many T-cell effector functions, through associating with and enhancing signaling by the T-cell receptor (TCR)-CD28 complex. The present study was designed to determine the role of TRAF3 in signaling via the B-cell antigen receptor (BCR). The BCR is crucial for antigen recognition, survival, proliferation, and antibody production, and defects in BCR signaling can promote abnormal survival of malignant B cells. Here, we show that TRAF3 is associated with both CD79B and the BCR-activated kinases Syk and Btk following BCR stimulation. BCR-induced phosphorylation of Syk and additional downstream kinases was increased in TRAF3−/− B cells, with regulation observed in both follicular and marginal zone B-cell subsets. BCR stimulation of TRAF3−/− B cells resulted in increased surface expression of MHC-II, CD80, and CD86 molecules. Interestingly, increased survival of TRAF3−/− primary B cells was resistant to inhibition of Btk, while TRAF3-deficient malignant B-cell lines showed enhanced sensitivity. TRAF3 serves to restrain normal and malignant BCR signaling, with important implications for its role in normal B-cell biology and abnormal survival of malignant B cells.
B-cell receptor (BCR) Btk cell signaling immunology inhibition mechanism lymphocyte lymphoma MAPK spleen tyrosine kinase (Syk) TNF receptor-associated factor (TRAF)

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