ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Functional redundancy of MyD88-dependent signaling pathways in a murine model of histidyl-transfer RNA synthetase-induced myositis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Single-cell RNA sequencing reveals clonally expanded CD4+ tissue-resident memory T cells in histidyl-tRNA synthetase-induced myositis.JCI insight · 2026Article
- IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Animal Models of Idiopathic Inflammatory Myopathies: Bridging Mechanistic Insights and Clinical Translation.International journal of molecular sciences · 2026Review
- Secreted mitochondrial aspartyl-tRNA synthetase (DARS2) regulates TNFα signaling.Physiological reports · 2025Article
- Spontaneous Remission in a Patient with Anti-OJ Autoantibodies-positive Anti-synthetase Syndrome Following SARS-CoV-2 Infection and mRNA Vaccination.Internal medicine (Tokyo, Japan) · 2025Article
- The foreign body response to biomaterial implants is reduced by co-inhibition of TLR2 and TLR4.Acta biomaterialia · 2025Article
- Clinical features associated with the presence of anti-Ro52 and anti-Ro60 antibodies in Jo-1 antibody-positive anti-synthetase syndrome.Frontiers in immunology · 2024Article
- Mechanistic perspectives on anti-aminoacyl-tRNA synthetase syndrome.Trends in biochemical sciences · 2023Review
- Antigen-driven T cell-macrophage interactions mediate the interface between innate and adaptive immunity in histidyl-tRNA synthetase-induced myositis.Frontiers in immunology · 2023Article
- Systemic Analysis of the Prognosis-Related RNA Alternative Splicing Signals in Melanoma.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- TLR expression in peripheral monocyte subsets of patients with idiopathic inflammatory myopathies: association with clinical and immunological features.Journal of translational medicine · 2020Article
- Roles of aminoacyl-tRNA synthetases in immune regulation and immune diseases.Cell death & disease · 2019Review
- Role of Jo-1 in the Immunopathogenesis of the Anti-synthetase Syndrome.Current rheumatology reports · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
We have previously shown that i.m. administration of bacterially expressed murine histidyl-tRNA synthetase (HRS) triggers florid muscle inflammation (relative to appropriate control proteins) in various congenic strains of mice. Because severe disease develops even in the absence of adaptive immune responses to HRS, we sought to identify innate immune signaling components contributing to our model of HRS-induced myositis. In vitro stimulation assays demonstrated HRS-mediated activation of HEK293 cells transfected with either TLR2 or TLR4, revealing an excitatory capacity exceeding that of other bacterially expressed fusion proteins. Corresponding to this apparent functional redundancy of TLR signaling pathways, HRS immunization of B6.TLR2(-/-) and B6.TLR4(-/-) single-knockout mice yielded significant lymphocytic infiltration of muscle tissue comparable to that produced in C57BL/6 wild-type mice. In contrast, concomitant elimination of TLR2 and TLR4 signaling in B6.TLR2(-/-).TLR4(-/-) double-knockout mice markedly reduced the severity of HRS-induced muscle inflammation. Complementary subfragment analysis demonstrated that aa 60-90 of HRS were absolutely required for in vitro as well as in vivo signaling via these MyD88-dependent TLR pathways--effects mediated, in part, through preferential binding of exogenous ligands capable of activating specific TLRs. Collectively, these experiments indicate that multiple MyD88-dependent signaling cascades contribute to this model of HRS-induced myositis, underscoring the antigenic versatility of HRS and confirming the importance of innate immunity in this system.
Indexed as
Identifiers
What OpenQuestion holds
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.