{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTNFRSF13B encodes TACI, a B cell–specific member of the tumor necrosis factor receptor superfamily that is critical for humoral immunity. TACI mediates the binding of the ligands BAFF and APRIL, which in turn drive immunoglobulin class switch recombination and isotype switching, especially toward IgG and IgA. Studies have shown that TACI is indispensable for proper B cell activation and differentiation, and that mutations in this gene are linked to primary immunodeficiencies such as common variable immunodeficiency (CVID) and selective IgA deficiency."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, TACI signaling involves a distinct cytoplasmic motif that, despite lacking a canonical TIR domain, recruits the adaptor molecule MyD88. This TLR‐like pathway activates downstream kinases such as IRAK1/4 and triggers NF‑κB signaling, ultimately upregulating activation‐induced cytidine deaminase (AID) to promote class switch recombination. In addition, alternative splicing generates TACI isoforms with differential ligand–binding properties that modulate plasma cell differentiation and B cell tolerance. Dysregulation—whether by haploinsufficiency or dominant interference of mutated receptors—can impair B cell responses, predisposing to autoimmunity as well as antibody deficiency."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its fundamental role in normal B cell biology, aberrant TACI signaling has been implicated in the pathogenesis of B cell malignancies and autoimmune disorders. In multiple myeloma and certain lymphomas, TACI levels correlate with the tumor cell’s dependency on the bone marrow microenvironment, and its engagement by BAFF/APRIL can regulate neoplastic cell survival and proliferation. These findings support the notion that modulation of TACI activity might represent a therapeutic target for intervening in diseases characterized by abnormal B cell expansion and function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, the complexity of TNFRSF13B mutations is mirrored by variable phenotypes. Heterozygous mutations often associate with antibody deficiency and autoimmunity, whereas biallelic changes may result in more pronounced hypogammaglobulinemia with a distinct lack of autoimmune manifestations. Large-scale investigations and genotype–phenotype studies in both adult and pediatric cohorts have underscored the crucial role of TACI in preserving B cell homeostasis and central tolerance, emphasizing the importance—and also the challenges—of TACI genetic screening in the evaluation and management of immune dysregulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Emanuela Castigli, Stephen A Wilson, Lilit Garibyan, et al. 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