ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Protective endogenous cyclic adenosine 5'-monophosphate signaling triggered by pemphigus autoantibodies.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- What protein kinases are crucial for acantholysis and blister formation in pemphigus vulgaris? A systematic review.Journal of cellular physiology · 2022Pooled it
- Plakoglobin phosphorylation at serine 665 is capable of stabilizing cadherin-mediated adhesion in keratinocytes.JCI insight · 2026Article
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- Epac1 contributes to apremilast-mediated rescue of pemphigus autoantibody-induced loss of keratinocyte adhesion.JCI insight · 2025Article
- [Phosphodiesterase 4 inhibitors in dermatology : Role in the treatment of skin diseases].Dermatologie (Heidelberg, Germany) · 2024Review
- Unbiased screening identifies regulators of cell-cell adhesion and treatment options in pemphigus.Nature communications · 2024Article
- Understanding Active Photoprotection: DNA-Repair Enzymes and Antioxidants.Life (Basel, Switzerland) · 2024Review
- Mouse models of pemphigus: valuable tools to investigate pathomechanisms and novel therapeutic interventions.Frontiers in immunology · 2023Review
- Autoantibody-Specific Signalling in Pemphigus.Frontiers in medicine · 2021Review
- Cardiomyocyte adhesion and hyperadhesion differentially require ERK1/2 and plakoglobin.JCI insight · 2020Article
- Case Report: Apremilast for Therapy-Resistant Pemphigus Vulgaris.Frontiers in immunology · 2020Article
- Dsg2 Upregulation as a Rescue Mechanism in Pemphigus.Frontiers in immunology · 2020Article
- [Therapy of pemphigus].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2019Review
- Synergy among non-desmoglein antibodies contributes to the immunopathology of desmoglein antibody-negative pemphigus vulgaris.The Journal of biological chemistry · 2019Article
- Role of Src and Cortactin in Pemphigus Skin Blistering.Frontiers in immunology · 2019Article
- Histamine causes endothelial barrier disruption via CaScientific reports · 2018Article
- Emerging treatment options for the management of pemphigus vulgaris.Therapeutics and clinical risk management · 2018Review
- A New Classification System for IgG4 Autoantibodies.Frontiers in immunology · 2018Review
- Different signaling patterns contribute to loss of keratinocyte cohesion dependent on autoantibody profile in pemphigus.Scientific reports · 2017Article
- Crosstalk between Signaling Pathways in Pemphigus: A Role for Endoplasmic Reticulum Stress in p38 Mitogen-Activated Protein Kinase Activation?Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Pemphigus vulgaris (PV) is an autoimmune skin disease mediated by autoantibodies directed against the cadherin-type cell adhesion molecules desmoglein (Dsg) 3 and Dsg1 and is characterized by loss of keratinocyte cohesion and epidermal blistering. Several intracellular signaling pathways, such as p38MAPK activation and RhoA inhibition, have been demonstrated to be altered following autoantibody binding and to be causally involved in loss of keratinocyte cohesion. In this paper, we demonstrate that cAMP-mediated signaling completely prevented blister formation in a neonatal pemphigus mouse model. Furthermore, elevation of cellular cAMP levels by forskolin/rolipram or β receptor agonist isoproterenol blocked loss of intercellular adhesion, depletion of cellular Dsg3, and morphologic changes induced by Ab fractions of PV patients (PV-IgG) in cultured keratinocytes. Incubation with PV-IgG alone increased cAMP levels, indicating that cAMP elevation may be a cellular response pathway to strengthen intercellular adhesion. Our data furthermore demonstrate that this protective pathway may involve protein kinase A signaling because protein kinase A inhibition attenuated recovery from PV-IgG-induced cell dissociation. Finally, cAMP increase interfered with PV-IgG-induced signaling by preventing p38MAPK activation both in vitro and in vivo. Taken together, our data provide insights into the cellular response mechanisms following pemphigus autoantibody binding and point to a possible novel and more specific therapeutic approach in pemphigus.
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Registered trials
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