ArticleNature communications2018
A proline deletion in IFNAR1 impairs IFN-signaling and underlies increased resistance to tuberculosis in humans.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 68 citations in OpenAlex.
- Trial
- Strong, sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.Cell host & microbe · 2026Article
- Monocytic niches escape T cell surveillance and promote Mycobacterium tuberculosis persistence in lymph nodes.Immunity · 2026Article
- Polymorphisms in IRF3 exon 1 influence the immune response to Brucella infection in small ruminants.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Strong sustained type I IFN signaling acts cell intrinsically to impair IFNγ responses and cause tuberculosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Monogenic disorders of immunity: Common variants are not so rare.Cell genomics · 2026Review
- Genome-wide screen inbioRxiv : the preprint server for biology · 2025Article
- Interferons in health and disease.Cell · 2025Review
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- A common form of dominant human IFNAR1 deficiency impairs IFN-α and -ω but not IFN-β-dependent immunity.The Journal of experimental medicine · 2025Article
- Immunological roads diverged: mapping tuberculosis outcomes in mice.Trends in microbiology · 2025Review
- Identification of amino acid residue in theJournal of virology · 2024Article
- Human Alveolar and Monocyte-Derived Human Macrophage Responses to Mycobacterium tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Type I interferon exacerbates Mycobacterium tuberculosis induced human macrophage death.EMBO reports · 2024Article
- Mycobacterial CpsA activates type I IFN signaling in macrophages via cGAS-mediated pathway.iScience · 2024Article
- Article
- Pathogenicity of Type I Interferons inInternational journal of molecular sciences · 2023Review
- Article
- Research progress on genetic control of host susceptibility to tuberculosis.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Review
- Immune evasion and provocation by Mycobacterium tuberculosis.Nature reviews. Microbiology · 2022Review
Corrections and comments
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type I interferons (IFN), best known for their anti-viral functions, have been shown to impair host resistance to intracellular bacteria in mice. However, the precise role of type I IFN signaling in bacterial infection in humans is unclear. Here, we show that genetic variation in the human IFNAR1 gene is associated with decreased susceptibility to tuberculosis and an increased risk of viral hepatitis in Chinese populations. Receptor mutagenesis and cell signaling studies establish that the IFNAR1 mutation corresponding to a proline deletion in the hinge region of the membrane-proximal domain of IFNAR1 decreases the binding affinity of IFNAR1 to IFN-β, impeding type I IFN signaling. Our findings suggest that IFNAR1 signaling underlies an increased risk of tuberculosis in humans and reveals a function for the IFNAR1 inter-domain region in cytokine-cytokine receptor interaction and signal transduction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.