ArticleThe Journal of clinical investigation1997
Glucocorticoid-mediated repression of cytokine gene transcription in human arteritis-SCID chimeras.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Treatment Guidance for Palmoplantar Pustulosis 2022.The Journal of dermatology · 2026Guideline
- Review
- Animal models for large vessel vasculitis - The unmet need.Rheumatology and immunology research · 2023Review
- Pathogenic role of monocytes/macrophages in large vessel vasculitis.Frontiers in immunology · 2022Review
- Functionally Heterogenous Macrophage Subsets in the Pathogenesis of Giant Cell Arteritis: Novel Targets for Disease Monitoring and Treatment.Journal of clinical medicine · 2021Review
- Glucocorticoids-All-Rounders Tackling the Versatile Players of the Immune System.Frontiers in immunology · 2019Review
- Ineffective levels of transforming growth factors and their receptor account for old age being a risk factor for Alzheimer's disease.Alzheimer's & dementia (New York, N. Y.) · 2019Review
- The characteristics of nivolumab-induced colitis: an evaluation of three cases and a literature review.BMC gastroenterology · 2018Review
- FDG-PET/CT(A) imaging in large vessel vasculitis and polymyalgia rheumatica: joint procedural recommendation of the EANM, SNMMI, and the PET Interest Group (PIG), and endorsed by the ASNC.European journal of nuclear medicine and molecular imaging · 2018Review
- Predictors of relapse and treatment outcomes in biopsy-proven giant cell arteritis: a retrospective cohort study.Rheumatology (Oxford, England) · 2016Article
- Endothelial Response to Glucocorticoids in Inflammatory Diseases.Frontiers in immunology · 2016Review
- Giant Cell Arteritis: Beyond Corticosteroids.Drugs & aging · 2015Review
- Serpin treatment suppresses inflammatory vascular lesions in temporal artery implants (TAI) from patients with giant cell arteritis.PloS one · 2015Article
- Biomarkers in vasculitis.Current opinion in rheumatology · 2014Review
- Immune mechanisms in medium and large-vessel vasculitis.Nature reviews. Rheumatology · 2013Review
- Design of the tocilizumab in giant cell arteritis trial.International journal of rheumatology · 2013Article
- Transient opening of the perineurial barrier for analgesic drug delivery.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- IFN-γ and IL-17: the two faces of T-cell pathology in giant cell arteritis.Current opinion in rheumatology · 2011Review
- Th17 and Th1 T-cell responses in giant cell arteritis.Circulation · 2010Article
- Vascular damage in giant cell arteritis.Autoimmunity · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Giant cell arteritis (GCA) is a vasculitic syndrome that preferentially affects medium and large-sized arteries. Glucocorticoid therapy resolves clinical symptoms within hours to days, but therapy has to be continued over several years to prevent disease relapses. It is not known whether and how glucocorticoids affect the function of the inflammatory infiltrate or why the disease persists subclinically despite chronic treatment. GCA is self-sustained in temporal arteries engrafted into SCID mice, providing a model in which the mechanisms of action and limitations of glucocorticoid therapy can be examined in vivo. Administration of dexamethasone to temporal artery-SCID chimeras for 1 wk induced a partial suppression of T cell and macrophage function as indicated by the reduced tissue concentrations of IL-2, IL-1beta, and IL-6 mRNA, and by the diminished expression of inducible NO synthase. In contrast, synthesis of IFN-gamma mRNA was only slightly decreased, and expression of TGF-beta1 was unaffected. These findings correlated with activation of the IkappaBalpha gene and blockade of the nuclear translocation of NFkappaB in the xenotransplanted tissue. Dose-response experiments suggested that steroid doses currently used in clinical medicine are suboptimal in repressing NFkappaB-mediated cytokine production in the inflammatory lesions. Chronic steroid therapy was able to deplete the T cell products IL-2 and IFN-gamma, whereas the activation of tissue-infiltrating macrophages was only partially affected. IL-1beta transcription was abrogated; in contrast, TGF-beta1 mRNA synthesis was steroid resistant. The persistence of TGF-beta1-transcribing macrophages, despite paralysis of T cell function, may provide an explanation for the chronicity of the disease, and may identify a novel therapeutic target in this inflammatory vasculopathy.
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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.