Ask about this productRelated genes to: IRF7 antibody
- Gene:
- IRF7 NIH gene
- Name:
- interferon regulatory factor 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-13
- Date modifiied:
- 2019-04-23
Related products to: IRF7 antibody
Related articles to: IRF7 antibody
- Duck plague, caused by the alphaherpesvirus Duck plague virus (DPV), is an acute, hemorrhagic, and economically devastating disease of waterfowl. DPV infection induces severe immunosuppression, yet the mechanisms by which this pathogen subverts host innate immunity, particularly through manipulation of the host ubiquitin system, remain unclear. The cGAS-STING signaling pathway is a cornerstone of anti-DNA viral immunity. In avian species, where IRF3 has been evolutionarily lost, the transcription factor IRF7 plays a pivotal role in activating type I interferons (IFN-I). Here, we identify duck RNF34 (DuRNF34) as a host E3 ubiquitin ligase that broadly suppresses the duck cGAS-STING pathway by targeting multiple components, including DucGAS, DuSTING, and DuIRF7, for ubiquitination and degradation. Importantly, DPV infection upregulates DuRNF34 expression, which selectively targets DuIRF7 for degradation to facilitate viral replication. Further affinity purification-mass spectrometry (AP-MS) analysis revealed that LORF2, a DPV-specific protein, recruits DuRNF34 to catalyze K11- and K48-linked polyubiquitination of DuIRF7 at lysine residues K51 and K453, leading to DuIRF7 degradation and suppression of IFN-β and downstream antiviral genes. Functional validation confirmed that siRNA-mediated knockdown of LORF2 markedly attenuated DPV-induced DuIRF7 degradation and impaired viral replication. Collectively, these findings reveal a novel immune evasion strategy in which DPV hijacks the host E3 ligase DuRNF34 via its unique protein LORF2, thereby targeting DuIRF7 for degradation to subvert innate immunity. This work provides new insights into herpesviral immune evasion and suggests potential targets for therapeutic intervention. - Source: PubMed
Publication date: 2026/04/24
Tian YanmingTian BinRan RanCai DongjieXiao ZhenWang MingshuWu YingYang QiaoZhang ShaqiuZhu DekangLiu MafengZhao XinxinSun DiHuang JuanOu XuminWu ZhenHe YuJia RenyongChen ShunCheng Anchun - Rheumatoid Arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction. Emerging evidence suggests that metabolic reprogramming plays a pivotal role in rheumatoid Arthritis (RA) pathogenesis. However, existing studies have focused predominantly on isolated pathways. This study aimed to systematically investigate the molecular interplay between metabolic reprogramming and immune dysregulation in RA. - Source: PubMed
Publication date: 2026/04/13
Cheng LinZong HexiangLi DongxuQian Long - Epstein-Barr virus (EBV), a member of gamma herpesvirus subfamily, infects more than 90% of the people in the world. There are some studies on EBV-mediated regulation of type I interferon (IFN-I) signaling, however, the underlying mechanism is still not fully understood. In this study, we demonstrated that the EBV encoded tegument protein BKRF4 could suppress RIG-I-like receptor (RLR) signaling pathway-induced IFN-β promoter activity and the mRNA transcription of IFN-β and downstream IFN-stimulated genes, which is favorable for RNA and DNA viral replications. Mechanically, BKRF4 was shown to interact with IRF3 and restrain its phosphorylation, dimerization, and nuclear translocation. Specifically, aa71-95 of BKRF4 was essential for its association with IRF3 and the inhibition of IFN-β promoter activity. Moreover, BKRF4 also could interplay with activated IRF7 but didn't affect the formation of IRF7 homodimer or IRF3/IRF7 heterodimer, yet it could impede the nuclear accumulation of IRF7. In addition, knockdown of BKRF4 during EBV lytic replication significantly enhanced IFN-β promoter activity and the phosphorylation and dimerization of IRF3. Taken together, our findings suggested that BKRF4 could negatively regulate the RLR-mediated IFN-β antiviral signaling, which provides new evidence for the molecular mechanism exploited by EBV to evade the host innate immunity. - Source: PubMed
Publication date: 2026/04/09
Li MeiliGao XinghongChen DannaHuang WenzhuoChen YuyuChen RuitongXu ZuoZhang YixiaoWang ShuaiWang KezhenXu ChunyanChen XinruPan ZhichengChi JiayiQin YangXie XiaoleiZhang JianPeng TaoChen ShengwenLv XiLi LinhaiLei ZhiweiChen YongerCai Mingsheng - Type I interferons (IFN-Is), including a single IFN-β and over a dozen IFN-αs, induce the anti-viral state. In vitro, IFN-β transcription requires the assembly of the "enhanceosome" composed of the constitutive transcription factors NF-κB and AP-1, and either constitutive IRF3 or IFN-I-inducible IRF7. IRF3 and IRF7 transcribe mouse IFN-α4 and human IFN-α1/13. Only IRF7 transcribes other IFN-αs. How IFN-I subtype multiplicity and their differential constitutive/IFN-I-inducible versus only IFN-I-inducible transcription help control viruses in vivo remains unknown. Using novel genetically modified mice, we demonstrate that most or all IFN-I subtypes, regardless of their transcriptional control, are necessary to curb the systemic dissemination of lymph-borne ectromelia virus (ECTV) but do not necessarily suppress ECTV or West Nile Virus (WNV) replication in the liver or the brain, or promote survival to their infection. Individually, the most critical IFN-I subtype to survive ECTV and WNV infections is IFN-β. IFN-α4 potentiates IFN-β but is not essential. PRDII, the IFN-β promoter's NF-κB binding site, which is required for enhanceosome assembly, is dispensable for in vivo IFN-β production but complements IRF7-IFN-β transcription to restrain ECTV and WNV. IFN-β alone protects IFN-α-deficient mice from ECTV but not from WNV lethality. Control of WNV replication in the brain successively requires IFN-α, IFN-β, and then PRDII-dependent IFN-β, suggesting that brain protection requires IFN-I production by various cell types and pathways. Thus, contrary to the prevailing view, in vivo, IFN-β does not function earlier than IFN-α, and IFN-I subtypes non-redundantly cooperate to restrain viruses in the periphery and in vital organs. - Source: PubMed
Publication date: 2026/04/08
Sigal Luisda Silva Carolina Rezende MeloHeath NatashaGelman MichelleKeller MeganChoi JihaeTang LingjuanTaiwo OluwatomilolaKafle SamitaTorres-Gonzalez EdilsonRamage HollyAndino RaulRoman Marisa - Owing to pivotal roles in CNS debris clearance and homeostasis, microglia are central targets for the therapy of neurodegenerative diseases. Intricate proximity to neurons, the inherent danger of neuroimmune toxicity, and intrinsically high plasticity and adaptability, impose high hurdles on microglia modulation. Attenuated viruses are being tested extensively against CNS malignancies (i.e., cancer virotherapy); yet, aside from viral vector-mediated payload delivery, virotherapy for non-neoplastic CNS disease remains unexplored. Here we report disseminated targeting of microglia with the highly attenuated polio:rhinovirus chimera, PVSRIPO, that culminated in profound, durable microglia reprogramming. This phenotype, rooted in extended cytoplasmic viral (v)RNA replication, was non-cytopathogenic and did not yield virus progeny or dissemination. vRNA replication in microglia triggered selective interferon (IFN) regulatory factor (IRF) 3/IRF7 transcriptional programs in the relative absence of NFκB-driven proinflammatory cytokine responses and elicited robust phagocytosis of both tumor cells and amyloid-beta. Targeting of microglia with PVSRIPO mediated immunotherapy in a mouse glioma model and the clearance of oligomeric amyloid-beta deposits in an injectable model of neurotoxic amyloid accumulation. This work identifies attenuated virotherapy as an approach to safely and effectively invigorate microglia function in immune surveillance and neurotoxic debris clearance. - Source: PubMed
Publication date: 2026/04/08
Carter Griffin PMcKay Zachary PKatz Mark ADisla LisbethNardone-White Dasean TSouthwell DerekBrown Michael CGromeier Matthias