ArticleThe Journal of clinical investigation1997
Development and characterization of desmoglein-3 specific T cells from patients with pemphigus vulgaris.
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 37 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
37 citing papers in PubMed, 177 citations in OpenAlex.
- Autoimmune bullous diseases: pathogenesis and clinical management.Molecular biomedicine · 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
- Cytokine profiling reveals HLA-linked Th2 and Th17 driven immune activation in pemphigus vulgaris patients and genetically susceptible healthy controls.Frontiers in immunology · 2024Article
- Healthy individuals genetically at-risk for the development of Pemphigus vulgaris or Alopecia areata share disease-like cytokine dysregulation.Frontiers in immunology · 2024Article
- T cell autoimmunity and immune regulation to desmoglein 3, a pemphigus autoantigen.The Journal of dermatology · 2023Review
- HLA class II antigens in Croatian patients with pemphigus vulgaris and their correlation with anti-desmoglein antibodies.Frontiers in immunology · 2023Article
- Understanding CD4Frontiers in immunology · 2023Review
- Article
- Autoimmune Pemphigus: Latest Advances and Emerging Therapies.Frontiers in molecular biosciences · 2021Review
- Article
- Article
- Common Denominators in the Immunobiology of IgG4 Autoimmune Diseases: What Do Glomerulonephritis, Pemphigus Vulgaris, Myasthenia Gravis, Thrombotic Thrombocytopenic Purpura and Autoimmune Encephalitis Have in Common?Frontiers in immunology · 2020Review
- Targeting interleukin 4 receptor α: A new approach to the treatment of cutaneous autoimmune bullous diseases?Dermatologic therapy · 2020Article
- Walnut antigens can trigger autoantibody development in patients with pemphigus vulgaris through a "hit-and-run" mechanism.The Journal of allergy and clinical immunology · 2019Article
- T helper type 1 polarizing γδ T cells and Scavenger receptors contribute to the pathogenesis of Pemphigus vulgaris.Immunology · 2018Article
- Analysis of Serum Cytokine Profile in Pemphigus.Annals of dermatology · 2017Article
- Pemphigus.Nature reviews. Disease primers · 2017Review
- Cytokine Indexes in Pemphigus Vulgaris: Perception of Its Immunpathogenesis and Hopes for Non-Steroidal Treatment.Iranian journal of pharmaceutical research : IJPR · 2017Article
- Mechanisms of Disease: Pemphigus and Bullous Pemphigoid.Annual review of pathology · 2016Review
- Overexpression of interleukin-23 and interleukin-17 in the lesion of pemphigus vulgaris: a preliminary study.Mediators of inflammation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pemphigus vulgaris (PV) is a cutaneous autoimmune disease characterized by blister formation in the suprabasilar layers of skin and mucosae and anti-desmoglein-3 (Dsg3) autoantibodies bound to the surface of lesional keratinocytes and circulating in the serum of patients. This disease can be reproduced in neonatal mice by passive transfer of patients' IgG, indicating that humoral immunity plays an important role in the pathogenesis of PV. Currently, the role of T lymphocytes in the development of PV is not clear. Here, we report that three immunoreactive segments of the ectodomain of Dsg3 specifically induced proliferation of T cells from PV patients. We found that T lymphocytes from 13 out of 14 patients responded to at least one of three Dsg3 peptides. T cells from controls and other patient groups did not respond to these Dsg3 peptides. The major T cell population stimulated by these Dsg3 peptides was CD4 positive. Dsg3-specific T cell lines and clones were developed and were shown to express a CD4 positive memory T cell phenotype. Upon stimulation, these cell lines and clones secreted a Th2-like cytokine profile. The Dsg3 responses of these T cells were restricted to HLA-DR, and not -DQ and -DP, of the major histocompatibility complex. This information will help to elucidate the cellular immune abnormalities leading to production of pathogenic IgG autoantibodies in patients with PV.
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.