ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Borrelia burgdorferi arthritis-associated locus Bbaa1 regulates Lyme arthritis and K/B×N serum transfer arthritis through intrinsic control of type I IFN production.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Development of a fluorescent reporter strain to facilitate studies ofMicrobiology spectrum · 2026Article
- Type I interferon signaling promotes early innate control ofbioRxiv : the preprint server for biology · 2026Article
- Evaluation of Immune Response Dynamics: Analyzing the Parameters of Complete Blood Count (CBC) in Experimental Borreliosis.Life (Basel, Switzerland) · 2025Article
- Aspects of the Immunopathogenesis of Lyme Arthritis.Microorganisms · 2025Review
- Article
- Antibody-mediated immunological memory correlates with long-term Lyme veterinary vaccine protection in mice.Vaccine · 2024Article
- Hitchhiker's Guide toJournal of bacteriology · 2024Review
- Impact ofFrontiers in immunology · 2024Article
- Borrelia burgdorferi Engages Mammalian Type I IFN Responses via the cGAS-STING Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Endogenous Linear Plasmids lp28-4 and lp25 Are Required for Infectivity and Restriction Protection in the Lyme Disease Spirochete Borrelia mayonii.Infection and immunity · 2023Article
- The Cdkn2a gene product p19 alternative reading frame (p19ARF) is a critical regulator of IFNβ-mediated Lyme arthritis.PLoS pathogens · 2022Article
- Functional Variants Associated WithFrontiers in genetics · 2022Article
- Lyme arthritis: linking infection, inflammation and autoimmunity.Nature reviews. Rheumatology · 2021Review
- Immune Response toCurrent issues in molecular biology · 2021Article
- Robust interferon signature and suppressed tissue repair gene expression in synovial tissue from patients with postinfectious, Borrelia burgdorferi-induced Lyme arthritis.Cellular microbiology · 2019Article
- The oncoprotein TBX3 is controlling severity in experimental arthritis.Arthritis research & therapy · 2019Article
- Induction of Interleukin 10 by Borrelia burgdorferi Is Regulated by the Action of CD14-Dependent p38 Mitogen-Activated Protein Kinase and cAMP-Mediated Chromatin Remodeling.Infection and immunity · 2018Article
- Genetic Control of Lyme Arthritis byJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- MicroRNA Expression Shows Inflammatory Dysregulation and Tumor-Like Proliferative Responses in Joints of Patients With Postinfectious Lyme Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- Antagonistic Interplay between MicroRNA-155 and IL-10 during Lyme Carditis and Arthritis.PloS one · 2015Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Localized upregulation of type I IFN was previously implicated in development of Borrelia burgdorferi-induced arthritis in C3H mice, and was remarkable due to its absence in the mildly arthritic C57BL/6 (B6) mice. Independently, forward genetics analysis identified a quantitative trait locus on Chr4, termed B. burgdorferi-associated locus 1 (Bbaa1), that regulates Lyme arthritis severity and includes the 15 type I IFN genes. Involvement of Bbaa1 in arthritis development was confirmed in B6 mice congenic for the C3H allele of Bbaa1 (B6.C3-Bbaa1), which developed more severe Lyme arthritis and K/B×N model of rheumatoid arthritis (RA) than did parental B6 mice. Administration of a type I IFN receptor blocking mAb reduced the severity of both Lyme arthritis and RA in B6.C3-Bbaa1 mice, formally linking genetic elements within Bbaa1 to pathological production of type I IFN. Bone marrow-derived macrophages from Bbaa1 congenic mice implicated this locus as a regulator of type I IFN induction and downstream target gene expression. Bbaa1-mediated regulation of IFN-inducible genes was upstream of IFN receptor-dependent amplification; however, the overall magnitude of the response was dependent on autocrine/paracrine responses to IFN-β. In addition, the Bbaa1 locus modulated the functional phenotype ascribed to bone marrow-derived macrophages: the B6 allele promoted expression of M2 markers, whereas the C3H allele promoted induction of M1 responses. This report identifies a genetic locus physically and functionally linked to type I IFN that contributes to the pathogenesis of both Lyme and RA.
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