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Critical Reviews™ in Immunology
Impact-faktor: 1.352 5-jähriger Impact-Faktor: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Druckformat: 1040-8401
ISSN Online: 2162-6472

Volumes:
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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v32.i4.10
pages 287-305

Regulatory Roles of the Tumor Necrosis Factor Receptor BCMA

Christine M. Coquery
Department of Microbiology, Immunology, & Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA, USA 22908
Loren D. Erickson
Department of Microbiology, Immunology, & Cancer Biology, University of Virginia School of Medicine, Charlottesville, VA, USA 22908; Beirne B. Carter Center for Immunology Research, University of Virginia School of Medicine, Charlottesville, VA, USA

ABSTRAKT

B cell maturation antigen (BCMA) is a tumor necrosis family receptor (TNFR) member that is predominantly expressed on terminally differentiated B cells and, upon binding to its ligands B cell activator of the TNF family (BAFF) and a proliferation inducing ligand (APRIL), delivers pro-survival cell signals. Thus, BCMA is mostly known for its functional activity in mediating the survival of plasma cells that maintain long-term humoral immunity. The expression of BCMA has also been linked to a number of cancers, autoimmune disorders, and infectious diseases that suggest additional roles for BCMA activity. Despite recent advances in our understanding of the roles for the related TNFR members BAFF-R and transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), the signaling pathway used by BCMA for mediating plasma cell survival as well as its putative function in certain disease states are not well understood. By examining the expression, regulation, and signaling targets of BCMA, we may gain further insight into this receptor and how it operates within cells in both health and disease. This information is important for identifying new therapeutic targets that may be relevant in treating diseases that involve the BAFF/APRIL cytokine network.