IgM to IgG Class Switching Is a Necessary Step for Pemphigus Phenotype Induction in Desmoglein 3-Specific B Cell Receptor Knock-in Mouse.
Adult
Aged
Animals
Autoimmunity
/ immunology
B-Lymphocytes
/ immunology
Desmoglein 3
/ genetics
Female
Gene Knock-In Techniques
Humans
Immunoglobulin Class Switching
/ immunology
Immunoglobulin G
/ genetics
Immunoglobulin M
/ genetics
Keratinocytes
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Middle Aged
Pemphigus
/ genetics
Receptors, IgG
/ genetics
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
01 02 2022
01 02 2022
Historique:
received:
09
08
2021
accepted:
22
11
2021
pubmed:
9
1
2022
medline:
10
2
2022
entrez:
8
1
2022
Statut:
ppublish
Résumé
Pemphigus vulgaris is an autoimmune blistering disease caused by IgG targeting desmoglein 3 (Dsg3), an adhesion molecule of keratinocytes. Anti-Dsg3 IgG production is prevented in healthy individuals, but it is unclear how Dsg3-specific B cells are regulated. To clarify the immunological condition regulating Dsg3-specific B cells, a pathogenic anti-Dsg3 Ig (AK23) knock-in mouse was generated. AK23 knock-in B cells developed normally without undergoing deletion or acquiring an anergic phenotype in vivo. The knock-in B cells showed Ca
Identifiants
pubmed: 34996836
pii: jimmunol.2100781
doi: 10.4049/jimmunol.2100781
doi:
Substances chimiques
Desmoglein 3
0
Dsg3 protein, mouse
0
Fcgr2b protein, mouse
0
Immunoglobulin G
0
Immunoglobulin M
0
Receptors, IgG
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
582-593Informations de copyright
Copyright © 2022 by The American Association of Immunologists, Inc.