Role of Dsg1- and Dsg3-Mediated Signaling in Pemphigus Autoantibody-Induced Loss of Keratinocyte Cohesion.
Autoantibodies
/ blood
Biomarkers
Calcium
/ metabolism
Cell Adhesion
/ immunology
Cell Line
Desmoglein 1
/ metabolism
Desmoglein 3
/ metabolism
Enzyme-Linked Immunosorbent Assay
ErbB Receptors
/ metabolism
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Humans
Immunoglobulin G
/ blood
Keratinocytes
/ immunology
Models, Biological
Pemphigus
/ diagnosis
Phenotype
Signal Transduction
CRISPR/Cas9
autoimmunity
desmoglein
keratinocytes
pemphigus
signaling
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2019
2019
Historique:
received:
21
02
2019
accepted:
03
05
2019
entrez:
11
6
2019
pubmed:
11
6
2019
medline:
10
9
2020
Statut:
epublish
Résumé
Pemphigus is an autoimmune dermatosis in which mucocutaneous blisters are induced primarily by autoantibodies against Desmoglein (Dsg) 1 and 3. Pemphigus vulgaris (PV) usually is associated with autoantibodies against Dsg3 whereas pemphigus foliaceus (PF) patients present autoantibodies against Dsg1. Several signaling pathways were proposed to cause loss of keratinocyte adhesion. However, relevance of different signaling pathways and role of Dsg1 and 3 to trigger signaling are not fully understood. Here, we show that Ca
Identifiants
pubmed: 31178865
doi: 10.3389/fimmu.2019.01128
pmc: PMC6543754
doi:
Substances chimiques
Autoantibodies
0
Biomarkers
0
DSG1 protein, human
0
DSG3 protein, human
0
Desmoglein 1
0
Desmoglein 3
0
Immunoglobulin G
0
EGFR protein, human
EC 2.7.10.1
ErbB Receptors
EC 2.7.10.1
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1128Références
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