ReviewCurrent rheumatology reports2003
The role of Jo-1 in the immunopathogenesis of polymyositis: current hypotheses.
Review in Current rheumatology reports, 2003. 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
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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, 30 citations in OpenAlex.
- Autoantibody levels in myositis patients correlate with clinical response during B cell depletion with rituximab.Rheumatology (Oxford, England) · 2016Trial
- Trial
- Predictors of clinical improvement in rituximab-treated refractory adult and juvenile dermatomyositis and adult polymyositis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Trial
- Subcutaneous immunoglobulins for the treatment of a patient with antisynthetase syndrome and secondary chronic immunodeficiency after anti-CD20 treatment: a case report.Journal of medical case reports · 2017Article
- Role of Jo-1 in the Immunopathogenesis of the Anti-synthetase Syndrome.Current rheumatology reports · 2015Review
- Rituximab in refractory idiopathic inflammatory myopathies and antisynthetase syndrome: personal experience and review of the literature.Immunologic research · 2013Review
- Interaction of HLA-DRB1*03 and smoking for the development of anti-Jo-1 antibodies in adult idiopathic inflammatory myopathies: a European-wide case study.Annals of the rheumatic diseases · 2012Article
- Plasmonic substrates for multiplexed protein microarrays with femtomolar sensitivity and broad dynamic range.Nature communications · 2011Article
- Antisynthetase syndrome.Current rheumatology reports · 2011Review
- Role of innate immunity in a murine model of histidyl-transfer RNA synthetase (Jo-1)-mediated myositis.Arthritis and rheumatism · 2011Article
- Sensitive and robust luminescent profiling of anti-La and other autoantibodies in Sjogren's syndrome.Autoimmunity · 2009Article
- Defining cancer risk in dermatomyositis. Part II. Assessing diagnostic usefulness of myositis serology.Clinical and experimental dermatology · 2009Review
- The diagnostic utility of myositis autoantibody testing for predicting the risk of cancer-associated myositis.Annals of the rheumatic diseases · 2007Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polymyositis represents an autoimmune disease in which T cells mediate destruction of muscle cells. Although the precise trigger(s) for this process remain unknown, distinct clinical subsets exist that are characterized by antibodies directed against specific nuclear and cytoplasmic antigens including Jo-1 (histidyl-transfer RNA synthetase). Coupled with a range of genetic and histomorphologic data, the stereotypical serologic response suggests that antigen-specific T cells directed against Jo-1 can promote T cell-mediated cytolysis of muscle cells as well as anti-Jo-1 antibody formation in selected patients with polymyositis. Beyond a previously developed animal model that has demonstrated the capacity of Jo-1 to promote humoral and cell-mediated immune responses leading to myositis, recent studies have revealed the existence of Jo-1-specific T cells in the peripheral blood of patients with Jo-1 antibody-positive polymyositis. Even more striking, investigators have discovered that Jo-1 can serve as a chemokine for immature dendritic cells and T lymphocytes. Collectively, these findings suggest a mechanism by which Jo-1 can bridge the innate and adaptive immune responses, leading to the breakdown of tolerance and autoimmune destruction of muscle.
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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.