期刊
CURRENT OPINION IN IMMUNOLOGY
卷 71, 期 -, 页码 124-131出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2021.06.014
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- Francis Crick Institute from Cancer Research UK [FC001194]
- UK Medical Research Council [FC001194]
- Wellcome Trust [FC001194]
BAFF is a critical cytokine for the survival of mature naïve B cells, memory B cells, autoimmune B cells, and malignant chronic lymphocytic leukaemia (CLL) cells by acting through the BAFFR receptor. The crosstalk between BAFFR and other receptors like B cell antigen receptor (BCR) plays a crucial role in the expansion of autoimmune and CLL cells. BAFF binding to BAFFR leads to degradation of TRAF3, relieving inhibition of SYK activity and transducing signals for B cell survival.
BAFF is a critical cytokine supporting the survival of mature naive B cells, acting through the BAFFR receptor. Recent studies show that BAFF and BAFFR are also required for the survival of memory B cells, autoimmune B cells as well as malignant chronic lymphocytic leukaemia (CLL) cells. BAFFR cooperates with other receptors, notably the B cell antigen receptor (BCR), a process which is critical for the expansion of autoimmune and CLL cells. This crosstalk may be mediated by TRAF3 which interacts with BAFFR and with CD79A, a signalling subunit of the BCR and the downstream SYK kinase, inhibiting its activity. BAFF binding to BAFFR leads to degradation of TRAF3 which may relieve inhibition of SYK activity transducing signals to pathways required for B cell survival. BAFFR activates both canonical and non-canonical NF-kappa B signalling and both pathways play important roles in the survival of B cells and CLL cells.
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