Ask about this productRelated genes to: IFNAR1 antibody
- Gene:
- IFNAR1 NIH gene
- Name:
- interferon alpha and beta receptor subunit 1
- Previous symbol:
- IFNAR
- Synonyms:
- IFRC
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: IFNAR1 antibody
Related articles to: IFNAR1 antibody
- People with triple-negative breast cancer (TNBC) typically have poorer survival than those with other breast cancer subtypes, with fewer treatment options available. Type I interferon (IFN) signaling has been reported as an important regulator of metastasis and therapeutic response in TNBC, but the off-target toxicity of IFN therapies has limited progression to clinical use. Augmenting Bone Morphogenetic Protein (BMP) signaling has also been associated with anti-metastatic effects, but BMP therapies are not clinically available presently. Tilorone is an anti-viral drug that induces IFN signaling, which has recently gained added attention as an enhancer of BMP signaling. As an agent capable of enhancing two mechanisms of interest, we therefore aimed to test the therapeutic effects of tilorone in preclinical models of metastatic breast cancer. - Source: PubMed
Publication date: 2026/05/07
Saunders Alastair A EMouchemore Kellie AVojtech LauraJames Lauren SChadwick Thomas BChi Lap HingKaragiannis ChrisBell CarolineThomson Rachel EParker Belinda SAnderson Robin LGregorevic Paul - Yellow fever virus (YFV) infection is life-threatening but preventable by the live-attenuated YFV 17D/17DD vaccine. Rare Adverse Events Following Immunization (AEFI-YF) involve Inborn Errors of Immunity (IEI), and auto-antibodies against type I interferons (IFNs). We conducted an integrative genetics and functional investigation of a Brazilian family with three siblings presenting AEFI-YF (two deceased), using whole exome sequencing (WES), and qPCR, molecular modeling, in vitro YFV-17D stimulation of leukocytes, cytokine quantification, immunophenotyping, and RNAseq. A novel homozygous IFNAR1 copy number variation (CNV Δ3-4-5) in the proband (heterozygous in five of 11 unaffected relatives) caused receptor dysfunction, suppressing baseline IFN responses but triggering inflammasome-driven innate cell activation upon YFV-17D exposure. This study underscores IFNAR1 deficiency's causality in AEFI-YF pathogenesis and provides mechanistical insights. Our findings advocate for precision vaccinology by screening relatives of AEFI-YF cases for type I IFN EIIs and auto-antibodies prior to live-attenuated vaccination. - Source: PubMed
Publication date: 2026/05/05
Azamor TamirisBastard Paulda Silva Andrea Marques Vieirade Almeida Machado LucasDos Santos Gonçalves BrennoJouanguy EmmanuelleZhang QianMelgaço Juliana GilCoelho Felipe Soaresda Rosa Lorenna CarvalhoTubarão Luciana NevesCunha Daniela Pradoda Silva Agonigi Bruna Nunesde Almeida Camila DiasPedro Renata SaraivaDos Santos Alves Nathaliade Moura Dias BrendaSchwarcz Waleska DiasGoudouris Ekaterini SimõesFonseca Dennyson Leandro MathiasCabral-Marques OtavioCasanova Jean-Laurentde Oliveira Patrícia Mouta NunesLourdes de Sousa Maia Maria deVasconcelos ZiltonBom Ana Paula Dinis Ano - Secondary bacterial pneumonia following influenza A virus (IAV) infection markedly exacerbates lung inflammation and contributes to acute respiratory distress syndrome (ARDS); however, the immunologic pathways that drive lung injury and determine protective versus pathogenic inflammation remain incompletely defined. Using a clinically relevant murine model of sublethal IAV infection followed by methicillin-resistant Staphylococcus aureus (MRSA) challenge under antibiotic therapy, this study investigated the dynamic role of type I interferon (IFN-I) signaling in disease progression. The findings demonstrate that IFN-I exerts dual and contrasting effects on the host inflammatory response: it enhances myeloid-derived TNF-α while indirectly suppressing T cell-derived IFN-γ. Reporter mouse models identified recruited monocytes and dendritic cells (DCs) as the primary IFN-I-targeted populations, whereas neutrophils, T cells, and alveolar macrophages exhibited limited direct responsiveness. Myeloid-specific deletion of IFNAR1 reduced TNF-α production, restrained inflammatory monocyte differentiation, and improved survival without disrupting IFN-γ and IL-10 balance. Temporal IFNAR1 blockade further revealed that early IFN-I signaling supports alveolar macrophage maintenance and primes monocytes/DCs for immune activation, whereas sustained signaling during bacterial superinfection drives persistent monocyte chemoattractant production, excessive monocyte activation, and delayed resolution of inflammation. Collectively, these findings position IFN-I as a temporal immune rheostat-protective during acute viral infection but pathogenic when prolonged-and define a therapeutic window in which selective IFNAR inhibition enhances host antibacterial defense, either alone or in combination with antibiotic therapy. These insights highlight a promising immunomodulatory strategy to improve outcomes in severe viral-bacterial pneumonia and ARDS. - Source: PubMed
Publication date: 2026/03/23
Uddin Md BashirMcKelvey MichaelPalani SunilShao ShengjunLiang YuejinSun Keer - Parkinson's disease (PD) is an age-related neurodegenerative disorder characterized by classical motor symptoms due to a loss of dopaminergic neurons in the substantia nigra . The type I interferons (IFNs) are elevated in the aging brain, and we have implicated them in the neuroinflammatory response in PD. With increasing evidence of gastrointestinal dysfunction in PD patients, this study explored the contribution of the type I IFNs to the transmission of pathology from the brain to the gut in PD. - Source: PubMed
Publication date: 2026/03/19
Waters HarrisonChen ShuyanVincan ElizabethFlanagan Dustin JSchwab Renate H MCrack Peter JTaylor Juliet M - Endometrial cancer (ECa) is one of the most common gynecologic malignancies, with limited therapeutic responses in metastatic or recurrent cases. The bacterial microbiota has emerged as a key modulator of carcinogenesis and antitumor immunity. However, the role of endometrial microbiota in ECa pathogenesis and prognosis remains poorly understood. - Source: PubMed
Publication date: 2026/04/20
Min KyungchanKim Se IkLee MinjiKim YunjaeJeong ChanyeongKim SujeongKim Sang JinKim HyunCho BeomkiJoo YanghyunPark HansooLee Maria