{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNFKBIZ encodes the atypical nuclear regulator IκB‑ζ, which plays a pivotal role in fine‐tuning NF‑κB–dependent gene expression. IκB‑ζ is uniquely induced by microbial products and proinflammatory cytokines such as interleukin‑1, IL‑17, and Toll‑like receptor ligands, and its expression is controlled by MyD88‐dependent pathways. Once induced, IκB‑ζ acts as a selective transcriptional coactivator that governs a subset of inflammatory mediators—including IL‑6, antimicrobial peptides like human β‑defensin‑2, and other cytokines important for host defence and immune homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, IκB‑ζ preferentially interacts with NF‑κB subunits—particularly with p50 homodimers—to form ternary complexes at promoter regions that contain both κB and additional regulatory binding sites (for example, C/EBP or Egr factors). This interaction can either potentiate or suppress transcription of NF‑κB target genes, depending on the cellular context and promoter architecture. Post‐transcriptional regulation of its mRNA by a 165‐nucleotide element and modulation by upstream regulators such as IRAK1/4 further ensure that IκB‑ζ expression is tightly controlled during inflammatory signalling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn vivo and ex vivo studies have revealed that IκB‑ζ is critical in the pathogenesis of several inflammatory and autoimmune disorders as well as in tissue remodelling processes. Its dysregulation is linked to chronic conditions such as psoriasis, ulcerative colitis, and aberrant immune responses in asthma and pneumococcal infection, while its expression is counterselected in certain cancers (for example, colorectal carcinogenesis and glioma progression). These findings indicate that IκB‑ζ not only modulates inflammation but also influences cell proliferation, survival, and differentiation in a tissue‐specific manner."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in chronic inflammation and autoimmunity, IκB‑ζ is also central to host defence against pathogens. It participates in antimicrobial responses—for instance, by regulating defensin gene expression in epithelial cells—and modulates key cytokine outputs such as interferon‑γ in natural killer cells. Genetic polymorphisms within NFKBIZ further associate with altered susceptibilities to invasive infections and even influence outcomes in conditions like COVID‑19, highlighting its potential as a therapeutic target in infectious and inflammatory diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Akiko Eto, Tatsushi Muta, Soh Yamazaki, et al. 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