Tumor necrosis factor receptor superfamily member 13B (TACI) (TACI)

Tumor necrosis factor receptor superfamily member 13B (TNFRSF13B), commonly known as TACI, is a transmembrane receptor primarily expressed on the surface of B-cells and plasma cells [UniProt: O14836]. It plays a critical role in the humoral immune response by binding to two key ligands: B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL). These interactions are essential for B-cell maturation, survival, and immunoglobulin isotype switching [PMID: 10956601]. Mutations in the TNFRSF13B gene are frequently associated with primary immunodeficiencies, such as common variable immunodeficiency (CVID) and IgA deficiency, while overactivity or dysregulation of the TACI pathway is linked to autoimmune diseases like systemic lupus erythematosus (SLE) and B-cell malignancies [PMID: 16007086]. Therapeutic strategies targeting TACI often involve decoy receptors or fusion proteins, such as Atacicept and Telitacicept, which neutralize BAFF and APRIL to reduce pathogenic B-cell activity [DrugBank: DB05054]. These therapies are currently being evaluated for their efficacy in treating autoimmune disorders and plasma cell dyscrasias.

Other names

TACICD267Transmembrane activator and CAML interactorTNFRSF13B

TNFRSF13B-targeted therapies typically function as soluble decoy receptors (fusion proteins) that bind to and neutralize the ligands BAFF (BLyS) and APRIL, thereby preventing them from interacting with their endogenous receptors (TACI, BCMA, and BAFF-R) and inhibiting B-cell-mediated autoimmune responses [PMID: 21454471].