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Tumor necrosis factor receptor superfamily member 17 (TNFRSF17), also known as B cell maturation antigen (BCMA), as well as TNFRSF13A TNFRSF17 (also known as TNFRSF13A, B cell maturation antigen or BCMA, CD269) is predominantly expressed on terminally differentiated B cells, including multiple myeloma cells, and is important for B cell development and autoimmune response. Upon binding to its ligands, B cell activator of the TNF family (BAFF, also known as TNSF13B, TALL-1, BLyS, zTNF4), and a proliferation inducing ligand (APRIL), BCMA activates NF-kappaB and MAPK8/JNK; it has a higher affinity for APRIL than for BAFF. This receptor may transduce signals for cell survival and proliferation by binding to TRAF1, TRAF2, and TRAF3. BCMA expression has also been linked to a number of cancers, autoimmune disorders, and infectious diseases. It has been shown that although BCMA does not play a role in normal B cell homeostasis, it is critical for the long-term survival of bone marrow plasma cells. BCMA is expressed in a number of hematologic malignancies, including both Hodgkin's and non-Hodgkin's lymphomas, as well as primary tumor cells and cell lines of multiple myeloma, playing a critical role in protecting myeloma cells from apoptosis. BCMA has been identified as a promising chimeric antigen receptor (CAR) target for multiple myeloma; CARs are synthetic transmembrane proteins used to redirect autologous T cells with a new specificity for antigens on the surface of cancer cells. BCMA may also be implicated in the context of both viral and fungal infections; peripheral blood B cells isolated from HIV+ viremic patients have increased expression levels of BCMA, and significant decreased levels are found during fungal infection with C. neoformans. BCMA has been linked to mucosal immunity; its signaling in B cells and non-B cells is important for driving protective IgA responses. Also, abnormal expression or signaling of BCMA in the gut may be relevant to diseases, such as irritable bowel disease and ulcerative colitis. |
Jiyao W et al.(2023). "The conserved domain database in 2023.",