Trial reportClinical and experimental immunology2015
T cell participation in autoreactivity to NC16a epitopes in bullous pemphigoid.
Trial report in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Racial and ethnic disparities in T helper 2-mediated inflammatory skin disorders.Skin health and disease · 2026Review
- Shared Mechanistic Pathways in Bullous Pemphigoid, Chronic Spontaneous Urticaria, Prurigo Nodularis, and Chronic Prurigo of Unknown Origin: Implications for Targeted Therapies.American journal of clinical dermatology · 2026Review
- Regulatory T cells in bullous pemphigoid: biological characteristics, dysfunction, and pathogenic roles.Frontiers in immunology · 2026Review
- Immunophenotypic and Transcriptomic Analysis of Peripheral Blood Mononuclear Cells in Bullous Pemphigoid.Annals of dermatology · 2025Article
- Autoimmune bullous diseases: pathogenesis and clinical management.Molecular biomedicine · 2025Review
- Bullous pemphigoid.Nature reviews. Disease primers · 2025Review
- JAK-STAT pathway, type I/II cytokines, and new potential therapeutic strategy for autoimmune bullous diseases: update on pemphigus vulgaris and bullous pemphigoid.Frontiers in immunology · 2025Review
- Characteristics and Risk Factors of Infections among Patients with Autoimmune Bullous Diseases: A Retrospective Single-Center Study in China.Infectious diseases & immunity · 2024Article
- Advancements in Bullous Pemphigoid Treatment: A Comprehensive Pipeline Update.American journal of clinical dermatology · 2024Review
- Exploring mechanisms of skin aging: insights for clinical treatment.Frontiers in immunology · 2024Review
- Understanding CD4Frontiers in immunology · 2023Review
- The cytokine milieu of bullous pemphigoid: Current and novel therapeutic targets.Frontiers in medicine · 2023Review
- Bullous pemphigoid: The role of type 2 inflammation in its pathogenesis and the prospect of targeted therapy.Frontiers in immunology · 2023Review
- Adaptive and innate immune pathogenesis of bullous pemphigoid: A review.Frontiers in immunology · 2023Review
- Study of cytokine-induced immunity in bullous pemphigoid: recent developments.Annals of medicine · 2023Review
- A Review of the Immunologic Pathways Involved in Bullous Pemphigoid and Novel Therapeutic Targets.Journal of clinical medicine · 2022Review
- Commentary: Efficacy and Safety of Dupilumab in Moderate-to-Severe Bullous Pemphigoid.Frontiers in immunology · 2021Article
- Thymic Stromal Lymphopoietin Is Implicated in the Pathogenesis of Bullous Pemphigoid by Dendritic Cells.Journal of immunology research · 2020Article
- Autoreactive T-Lymphocytes in Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Skin Barrier and Autoimmunity-Mechanisms and Novel Therapeutic Approaches for Autoimmune Blistering Diseases of the Skin.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bullous pemphigoid is a blistering skin disease characterized by autoantibodies against the NC16a domain of bullous pemphigoid 180. This study was performed to characterize and map the fine specificity of T cell responses to NC16a. Peripheral blood mononuclear cells (PBMC) from a total of 28 bullous pemphigoid patients and 14 matched controls were tested for proliferative and cytokine responses to recombinant NC16a and a complete panel of 21 overlapping peptides spanning this region of BP180. Proliferative responses to NC16A and the peptide panel in the patients with active disease were similar in frequency and magnitude to those in healthy donors, and included late responses typical of naive cells in approximately 60% of each group. Interleukin (IL)-4 responses were slightly stronger for six peptides, and significantly stronger for Nc16a, in patients than in controls. Factor analysis identified factors that separate responses to the peptide panel discretely into IL-4, T helper type 2 (Th2) pattern, interferon (IFN)-γ, Th1 pattern and IL-10 or transforming growth factor [TGF-β, regulatory T cell (Treg )] pattern. Factors segregating IL-10 versus IFN-γ were predicted by active blistering or remission, and TGF-β or IL-10 versus IFN-γ by age. Finally, we confirmed a significant up-regulation of IgE responses to BP180 in the patients with pemphigoid. This shows the complexity of T cell phenotype and fine autoreactive specificity in responses to NC16A, in patients and in normal controls. Important disease-associated factors determine the balance of cytokine responses. Of these, specific IL-4 and IgE responses show the strongest associations with pemphigoid, pointing to an important contribution by Th2 cytokines to pathogenesis.
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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.