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Transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI), also known as TNFRSF13B, is a member of the tumor necrosis factor receptor superfamily primarily expressed on the surface of B-cells and plasma cells. It serves as a critical regulator of the adaptive immune response by binding to two key ligands: B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) [UniProt: O14836]. These interactions are essential for B-cell maturation, immunoglobulin isotype switching, and the long-term survival of antibody-secreting plasma cells [PubMed: 11526139]. Dysregulation of TACI signaling is associated with several clinical conditions; for instance, mutations in the TNFRSF13B gene are a common genetic cause of common variable immunodeficiency (CVID) [PubMed: 16007086]. Conversely, overactivation or overexpression of TACI is implicated in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE) and B-cell malignancies such as multiple myeloma [PubMed: 33003316]. Therapeutic strategies targeting this pathway often utilize soluble decoy receptors, such as Atacicept and Telitacicept, which sequester BAFF and APRIL to prevent them from activating TACI and other related receptors [PubMed: 33003316]. These drugs are currently being investigated for their potential to treat autoimmune disorders and plasma cell dyscrasias by reducing B-cell hyperactivity and autoantibody production.
Soluble decoy receptor that binds and neutralizes BAFF and APRIL ligands to inhibit B-cell activation and survival.
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