Trial reportThe Journal of clinical investigation1999
Epidermal HLA-DR and the enhancement of cutaneous reactivity to superantigenic toxins in psoriasis.
Trial report in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 71 citations in OpenAlex.
- Development and validation of a prediction model for the risk of relapse in psoriasis.Scientific reports · 2026Article
- Article
- Triggers for the onset and recurrence of psoriasis: a review and update.Cell communication and signaling : CCS · 2024Review
- Berry Extracts and Their Bioactive Compounds Mitigate LPS and DNFB-Mediated Dendritic Cell Activation and Induction of Antigen Specific T-Cell Effector Responses.Antioxidants (Basel, Switzerland) · 2023Article
- Infection-provoked psoriasis: Induced or aggravated (Review).Experimental and therapeutic medicine · 2021Review
- Ghrelin protects against contact dermatitis and psoriasiform skin inflammation by antagonizing TNF-α/NF-κB signaling pathways.Scientific reports · 2019Article
- Verruciform xanthoma: A view on the concepts of its etiopathogenesis.Journal of oral and maxillofacial pathology : JOMFP · 2013Review
- [Psoriatic arthritis : a permanent challenge for rheumatologists and patients--Part 1: epidemiology, pathogenesis and clinical course].Zeitschrift fur Rheumatologie · 2011Review
- Activity of Antimicrobial Peptides and Conventional Antibiotics against Superantigen Positive Staphylococcus aureus Isolated from the Patients with Neoplastic and Inflammatory Erythrodermia.Chemotherapy research and practice · 2011Article
- [The role of streptococci in psoriasis].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2009Review
- Role of bacterial pathogens in atopic dermatitis.Clinical reviews in allergy & immunology · 2007Review
- Immunopathogenesis of psoriasis.Clinical reviews in allergy & immunology · 2007Review
- Role of staphylococcal superantigen in atopic dermatitis: influence on keratinocytes.Journal of Korean medical science · 2006Article
- Peripheral blood T cell responses to keratin peptides that share sequences with streptococcal M proteins are largely restricted to skin-homing CD8(+) T cells.Clinical and experimental immunology · 2004Article
- Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities.The Journal of clinical investigation · 2004Review
- Skin innate immune system in psoriasis: friend or foe?The Journal of clinical investigation · 1999Review
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
Abstract
Streptococcal and staphylococcal superantigens (SAg's) have been implicated in the pathogenesis of inflammatory skin diseases, but the mechanisms by which these toxins act are unknown. The present study assessed the ability of nanogram quantities of topically applied purified toxic shock syndrome toxin-1 (TSST-1), staphylococcal enterotoxin type B, and streptococcal pyrogenic enterotoxin types A and C to induce inflammatory reactions in clinically uninvolved skin of normal controls and subjects with psoriasis, atopic dermatitis, and lichen planus. These SAg's triggered a significantly greater inflammatory skin response in psoriatics than in normal control subjects or in subjects with atopic dermatitis or lichen planus. Surprisingly, skin biopsies did not exhibit the T-cell receptor Vbeta stimulatory properties predicted for SAg-induced skin reactions. By 6 hours after patch testing with SAg's, TNF-alpha mRNA had increased in the epidermis (but not the dermis) in biopsies from psoriatics, compared with controls. Immunohistochemical studies revealed significantly higher HLA-DR expression in keratinocytes from psoriatics than from controls. However, a mutant TSST-1 protein that fails to bind HLA-DR did not elicit an inflammatory skin reaction. These results indicate that keratinocyte expression of HLA-DR enhances inflammatory skin responses to SAg's. They may also account for previous studies failing to demonstrate selective expansion of T-cell receptor Vbetas in psoriatics colonized with SAg-producing Staphylococcus aureus, and they identify a novel T cell-independent mechanism by which SAg's contribute to the pathogenesis of inflammatory skin diseases.
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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.