ReviewClinical reviews in allergy & immunology2018
Pemphigus: a Comprehensive Review on Pathogenesis, Clinical Presentation and Novel Therapeutic Approaches.
Review in Clinical reviews in allergy & immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed, 186 citations in OpenAlex.
- FcRn Antagonism Leads to a Decrease of Desmoglein-Specific B Cells: Secondary Analysis of a Phase 2 Study of Efgartigimod in Pemphigus Vulgaris and Pemphigus Foliaceus.Frontiers in immunology · 2022Trial
- New-Onset Pemphigus Following Drug Exposure and Vaccination: A Systematic Review of Reported Cases.Vaccines · 2026Review
- Article
- Scalp Involvement In Pemphigus: A Retrospective Cohort Study Of Clinical And Immunopathologic Features.Dermatology practical & conceptual · 2026Article
- CellAwareGNN: Single-Cell Enhanced Knowledge Graph Foundation Model for Drug Indication Prediction.bioRxiv : the preprint server for biology · 2026Article
- Plakoglobin phosphorylation at serine 665 is capable of stabilizing cadherin-mediated adhesion in keratinocytes.JCI insight · 2026Article
- Paraneoplastic Pemphigus and Liver Biopsy Needle Track Dissemination in Hepatocellular Carcinoma: A Case Report.GE Portuguese journal of gastroenterology · 2026Article
- Dihydroartemisinin attenuates pemphigus vulgaris by regulating Dsg3 and the TLR9/NF-κB pathway.American journal of translational research · 2026Article
- Clinical and Immunological Outcomes of Rituximab Therapy in Pemphigus: A Prospective Observational Study.Dermatology (Basel, Switzerland) · 2026Observational
- Palliative oncodermatology: Management of malignancy-related cutaneous symptoms in the palliative care setting.Journal of the American Academy of Dermatology · 2025Review
- Juvenile pemphigus vulgaris: A narrative review.Medicine · 2025Review
- Feline immune-mediated skin disorders: Part 1.Journal of feline medicine and surgery · 2025Review
- Meeting report - Alpine desmosome disease meeting 2024: advances and emerging topics in desmosomes and related diseases.Journal of cell science · 2025Article
- 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
- Diversity and Epitope Spreading of Anti-RNA Polymerase III Antibodies in Systemic Sclerosis: A Potential Biomarker for Skin and Lung Involvement.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Conjoint analysis of methylation, transcriptomic, and proteomic profiles in pemphigus vulgaris.Orphanet journal of rare diseases · 2024Article
- Trends in disease severity and quality of life outcome measures in pemphigus clinical trials: A scoping review.Skin health and disease · 2024Article
- Gut Microbiome Dysbiosis in Patients with Pemphigus and Correlation with Pathogenic Autoantibodies.Biomolecules · 2024Article
- Article
- Gingival Manifestations in Oral Chronic Autoimmune Bullous Diseases: A Retrospective Study.Medicina (Kaunas, Lithuania) · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Pemphigus is a group of rare, potentially devastating autoimmune diseases of the skin and mucous membranes with high morbidity and potentially lethal outcome. The major clinical variant, pemphigus vulgaris (PV) is caused by a loss of intercellular adhesion of epidermal keratinocytes which is induced by IgG autoantibodies against components of desmosomes. Specifically, IgG against the desmosomal adhesion proteins, desmoglein 3 (Dsg3) and desmoglein 1 (Dsg1), preferentially target their ectodomains which are presumably critical for the transinteraction and signalling function of these adhesion molecules. There is a close immunogenetic association of PV with the human leukocyte antigen (HLA) class II alleles, HLA-DRB1*04:02 and HLA-DQB1*05:03. These have been shown to be critical for the presentation of immunodominant peptides to autoreactive CD4+ T helper cells. The importance of autoaggressive T-B cell interaction in the induction of pathogenic IgG autoantibodies which directly cause epidermal loss of adhesion has been demonstrated both clinically (by the use of the anti-CD20 monoclonal antibody rituximab) and experimentally (in PV mouse models). The strong association of clinically active pemphigus with autoantibodies of the IgG
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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.