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Canonically, the transcription factor interferon regulatory factor 5 (IRF5) is a key mediator of innate and adaptive immunity downstream of pathogen recognition receptors such as Toll-like receptors (TLRs). Hence, dysregulation of IRF5 function has been widely implicated in inflammatory and autoimmune diseases. Over the last few decades, dysregulation of IRF5 expression has been also reported in hematologic malignancies and solid cancers that support a role for IRF5 in malignant transformation, tumor immune regulation, clinical prognosis, and treatment response. This review will provide an in-depth overview of the current literature regarding the mechanisms by which IRF5 functions as either a tumor suppressor or oncogene, its role in metastasis, regulation of the tumor-immune microenvironment, utility as a prognostic indicator of disease, and new developments in IRF5 therapeutics that may be used to remodel tumor immunity.
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http://dx.doi.org/10.1016/j.bbcan.2023.189061 | DOI Listing |
Biochem Biophys Res Commun
August 2025
Intensive Care Unit, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan, 430061, Hubei, China; Hubei Province Academy of Traditional Chinese Medicine, Wuhan, 430061, Hubei, China. Electronic address:
Background: Coxsackievirus B3 (CVB3) infection is a common cause of myocarditis, and the resulting inflammatory response and cellular damage can lead to severe cardiac dysfunction. Astragaloside IV (AS-IV), a natural compound with anti-inflammatory and antiviral properties, has shown potential therapeutic value in various inflammatory and immune-related diseases. Our study aims to explore the potential effects and underlying mechanisms of AS-IV in CVB3-induced viral myocarditis (VMC).
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Institute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Germany.
Chronic pain (CP) is a major health issue globally, affecting millions and resulting in a significant healthcare burden. Although amitriptyline is widely used to manage CP, its immunomodulatory effects during pain therapy, especially on T cell phenotypes, remain unclear. In this study, we explored how amitriptyline alters T cell phenotypes in CP patients.
View Article and Find Full Text PDFCell Rep
September 2025
Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China; Pôle de Recherches Sino-Français en Science du Vivant et Gé
RNA helicase DDX3X is generally implicated in inflammasome activation and anti-viral responses. We characterize the common features of scattered DDX3X mutations in lymphoid cancers using molecular dynamics simulation and crystallization, thereby demonstrating their crucial role in Epstein-Barr virus (EBV) lytic gene-driven oncogenic processes. The DDX3X mutation is significantly related to impaired stimulator of interferon genes (STING)/ interferon regulatory factor 7 (IRF-7)/interferon (IFN)-α/β-mediated innate immunity, overexpression of EBV lytic gene BNLF2b, and increased formation of R-loops.
View Article and Find Full Text PDFEur J Pharmacol
September 2025
Department of Dermatology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China; Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education, Hefei, Anhui, China; Institute of Dermatology, Anhui Medical University, Hefei 230032, Anhui, China. Electronic
Vascular endothelial cells (ECs) damage is closely related to kidney injury. Our previous research revealed the involvement of interferon regulatory factor 1 (IRF1)-mediated PANoptosis of renal ECs in trichloroethylene (TCE)-induced immune kidney injury. However, how IRF1 regulates ECs PANoptosis remains unclear.
View Article and Find Full Text PDFInt J Biol Macromol
September 2025
College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu Province, China; Joint International Research Laboratory of Agriculture and Agri-Product Safety, the Ministry of Education of China, Yangzhou University, Yangzhou, Jiangsu Province, China; Jiangsu Co-Innovation Center for Prevent
African swine fever virus (ASFV) encodes multiple proteins to achieve immune escape, thereby disrupting the host's antiviral defense. This study demonstrates that the ASFV-encoded pE248R protein disrupted the Retinoic Acid-Inducible Gene I (RIG-I) mediated antiviral signaling cascade through dual regulatory mechanisms. Mechanistically, pE248R interacted with the caspase activation and recruitment domains (CARD) of RIG-I, effectively blocking its interaction with the mitochondrial adaptor MAVS.
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