{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNLRC5 functions as a pivotal modulator of innate immune responses. Several studies have demonstrated that NLRC5 negatively regulates the NF‑κB pathway and type I interferon signaling by interfering with key components such as the IKK complex and RIG‑I/MDA5, thereby dampening proinflammatory cytokine production. In addition, NLRC5 influences inflammasome activity and antiviral defenses, acting through mechanisms that include its dynamic ubiquitination and subsequent modulation of signaling complexes. These findings collectively position NLRC5 as a negative regulator that maintains immune homeostasis during microbial infections and inflammatory challenges."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its regulatory role in immune signaling, NLRC5 has emerged as an essential transcriptional coactivator of major histocompatibility complex (MHC) class I genes. By associating with promoter elements and cooperating with factors such as the RFX complex, NLRC5 orchestrates the expression of MHC class I molecules and related antigen‐processing components. This function is critical for the effective presentation of antigens, thereby influencing both antiviral immunity and anti-tumor immune surveillance. Notably, NLRC5 induction by interferon‑gamma further highlights its role in linking innate and adaptive immune responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDysregulation of NLRC5 is also implicated in oncogenesis and fibrogenesis. Aberrant expression or genetic/epigenetic alterations in NLRC5 have been associated with tumor immune evasion in various cancers, including hepatocellular carcinoma, renal cell carcinoma, and breast cancer. Moreover, NLRC5 has been shown to modulate cell proliferation, migration, and invasion in cancer cells, and to influence extracellular matrix production and tissue fibrosis in settings such as liver, renal, and dermal fibrotic disorders. These studies underscore the dual role of NLRC5 in promoting tumor progression while also modulating profibrogenic signaling pathways such as TGF‑β/Smad and PI3K/AKT."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence further indicates that NLRC5 serves as a multifunctional hub in a wide range of pathological conditions. Structural studies have unraveled unique features of NLRC5’s effector domains that distinguish it from other NLRs, enriching our understanding of its interaction with signaling partners. In parallel, altered NLRC5 expression and function have been linked to diverse disorders—including acute kidney injury, cerebral ischemia, gynecological conditions such as leiomyoma and endometriosis, periodontitis, and IgA nephropathy—as well as central nervous system diseases. 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