Fcγ Receptor IIB Controls Skin Inflammation in an Active Model of Epidermolysis Bullosa Acquisita.
Fcγ receptor
IgG
animal model
autoimmunity
epidermolysis bullosa acquisita
neutrophils
pemphigoid disease
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:
22
06
2019
accepted:
09
12
2019
entrez:
30
1
2020
pubmed:
30
1
2020
medline:
18
11
2020
Statut:
epublish
Résumé
Epidermolysis bullosa acquisita (EBA) is an autoimmune skin blistering disease characterized by IgG autoantibodies (aAb) against type VII collagen (COL7). The mechanisms controlling the formation of such aAbs and their effector functions in the skin tissue are incompletely understood. Here, we assessed whether the inhibitory IgG Fc receptor, FcγRIIB, controls the development of autoimmune skin blistering disease in an active model of EBA. For this purpose, we immunized congenic EBA-susceptible B6.SJL-H2s (B6.s) and B6.s-
Identifiants
pubmed: 31993051
doi: 10.3389/fimmu.2019.03012
pmc: PMC6971089
doi:
Substances chimiques
Autoantibodies
0
Autoantigens
0
Collagen Type VII
0
Fcgr2b protein, mouse
0
Receptors, IgG
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3012Informations de copyright
Copyright © 2020 Kovacs, Tillmann, Freund, Nimmerjahn, Sadik, Bieber, Ludwig, Karsten and Köhl.
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