ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Deficiency of type I IFN receptor in lupus-prone New Zealand mixed 2328 mice decreases dendritic cell numbers and activation and protects from disease.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 123 citations in OpenAlex.
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- The path ahead for understanding Toll-like receptor-driven systemic autoimmunity.Current opinion in immunology · 2024Review
- EGFR-ErbB2 dual kinase inhibitor lapatinib decreases autoantibody levels and worsens renal disease in Interferon α-accelerated murine lupus.International immunopharmacology · 2024Article
- Integrin αvβ3 Limits Cytokine Production by Plasmacytoid Dendritic Cells and Restricts TLR-Driven Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- The Role of the Oxidative State and Innate Immunity Mediated by TLR7 and TLR9 in Lupus Nephritis.International journal of molecular sciences · 2023Review
- Impaired dynamic X-chromosome inactivation maintenance in T cells is a feature of spontaneous murine SLE that is exacerbated in female-biased models.Journal of autoimmunity · 2023Article
- Breaking down the cellular responses to type I interferon neurotoxicity in the brain.Frontiers in immunology · 2023Review
- Article
- Spontaneous CD4+ T Cell Activation and Differentiation in Lupus-Prone B6.Nba2 Mice Is IFNAR-Independent.International journal of molecular sciences · 2022Article
- Interferon Lambda Regulates Cellular and Humoral Immunity in Pristane-Induced Lupus.International journal of molecular sciences · 2021Article
- Review
- Genetic and chemical inhibition of IRF5 suppresses pre-existing mouse lupus-like disease.Nature communications · 2021Article
- Meant to B: B cells as a therapeutic target in systemic lupus erythematosus.The Journal of clinical investigation · 2021Review
- Frontline Science: CD40 signaling restricts RNA virus replication in Mϕs, leading to rapid innate immune control of acute virus infection.Journal of leukocyte biology · 2021Article
- Inhibition of B cell activation followingJournal of translational autoimmunity · 2021Article
- The peptide symporter SLC15a4 is essential for the development of systemic lupus erythematosus in murine models.PloS one · 2021Article
- Essential role and therapeutic targeting of the glomerular endothelial glycocalyx in lupus nephritis.JCI insight · 2020Article
- Are lupus animal models useful for understanding and developing new therapies for human SLE?Journal of autoimmunity · 2020Review
- Plasmacytoid Dendritic Cells and Type I Interferon Promote Extrafollicular B Cell Responses to Extracellular Self-DNA.Immunity · 2020Article
- Type II but Not Type I IFN Signaling Is Indispensable for TLR7-Promoted Development of Autoreactive B Cells and Systemic Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Type I IFNs are potent regulators of innate and adaptive immunity and are implicated in the pathogenesis of systemic lupus erythematosus. Here we report that clinical and pathological lupus nephritis and serum anti-nuclear Ab levels are greatly attenuated in New Zealand Mixed (NZM) 2328 mice deficient in type I IFN receptors (IFNAR). To determine whether the inflammatory environment in NZM 2328 mice leads to IFNAR-regulated changes in dendritic cells (DC), the number, activation, and function of DC subsets were compared in 2- and 5-mo-old (clinically healthy) female NZM and NZM-IFNAR(-/-) mice. Numbers of activated CD40(high) plasmacytoid DC (pDC) were significantly increased in renal lymph nodes of 2-mo-old NZM but not NZM-IFNAR(-/-) mice, suggesting an early IFNAR-dependent expansion and activation of pDC at disease sites. Relative to NZM spleens, NZM-IFNAR(-/-) spleens in 5-mo-old mice were significantly decreased in size and contained reduced numbers of conventional DC subsets, but not pDC. Splenic and renal lymph node NZM-IFNAR(-/-) DC analyzed directly ex vivo expressed significantly less CD40, CD86, and PDL1 than did NZM DC. Upon activation with synthetic TLR9 ligands in vitro, splenic NZM-IFNAR(-/-) DC produced less IL-12p40/70 and TNF-alpha than did NZM DC. The limited IFNAR(-/-) DC response to endogenous activating stimuli correlated with reduced numbers of splenic activated memory CD4(+) T cells and CD19(+) B cells in older mice. Thus, IFNAR signaling significantly increases DC numbers, acquisition of Ag presentation competence, and proinflammatory function before onset of clinically apparent lupus disease.
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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.