Abstract
B-lymphocyte homeostasis depends on exogenous signals for survival during development and in immune responses to invading pathogens. These signals are continually provided by either tonic or antigen-mediated BCR signals and other trophic factors. B-cell-activating factor (BAFF) has emerged as a key growth factor for B lymphocytes. Through its interaction with a TNF-R family member, BAFF-R or BR3, BAFF promotes survival of both immature and mature B cells. BAFF/BR3 interaction also facilitates BCR-induced B-cell proliferation. Thus, dysregulation of the signals emanating from these receptors leads to autoimmune disease, whereas interference with these signals leads to B-cell immunodeficiencies. Multiple signal transduction pathways, including those involving transcription factor NF-κB, appear to play critical roles in BAFF-mediated B-cell biological responses. Recent studies have revealed that BR3 and BCR are functionally linked and that Bruton’s cytoplasmic tyrosine kinase (Btk)/NF-κB signaling plays an essential role in this process. Therefore, the primary objective of this article is to discuss BR3-signaling pathways, and the cooperation with BCR signals, that regulate B-cell survival during development and activation.
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Khan, W.N., Shinners, N.P., Castro, I., Hoek, K.L. (2009). BAFF Receptor Regulation of Peripheral B-Lymphocyte Survival and Development. In: Cancro, M. (eds) BLyS Ligands and Receptors. Contemporary Immunology. Humana Press. https://doi.org/10.1007/978-1-60327-013-7_2
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DOI: https://doi.org/10.1007/978-1-60327-013-7_2
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