ArticleThe Journal of investigative dermatology2025
Pemphigus Vulgaris Autoantibodies Induce an Endoplasmic Reticulum Stress Response.
Article in The Journal of investigative dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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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.
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Who cites it
3 citing papers in PubMed.
- Cadherin regulation of endoplasmic reticulum-plasma membrane contact sites.Cell reports · 2026Article
- Adapting upright light sheet fluorescence microscopy for imaging at air-liquid interface.Npj imaging · 2026Article
- Adapting Upright Light Sheet Fluorescence Microscopy for Imaging at Air-Liquid Interface.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Desmosomes are intercellular junctions that mediate cell-cell adhesion and are essential for maintaining tissue integrity. Pemphigus vulgaris (PV) is an autoimmune epidermal blistering disease caused by autoantibodies (IgG) targeting desmoglein 3, a desmosomal cadherin. PV autoantibodies cause desmosome disassembly and loss of cell-cell adhesion; however, the molecular signaling pathways that regulate these processes are not fully understood. Using high-resolution time-lapse imaging of live keratinocytes, we found that endoplasmic reticulum (ER) tubules make frequent and persistent contacts with internalizing desmoglein 3 puncta in keratinocytes treated with IgG of patients with PV. Biochemical experiments demonstrated that PV IgG activated ER stress signaling pathways, including both IRE1⍺ and PERK pathways, in cultured keratinocytes. Furthermore, ER stress transcripts were upregulated in the skin of patients with PV. Pharmacological inhibition of ER stress protects against PV IgG-induced desmosome disruption and loss of keratinocyte cell-cell adhesion, suggesting that ER stress may be an important pathomechanism and a therapeutically targetable pathway for PV treatment. These data support a model in which desmosome adhesion is integrated with ER function to serve as a cell adhesion stress sensor that is activated in blistering skin diseases.
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