IgA glycosylation and immune complex formation in IgAN.
APRIL
Aberrantly glycosylated IgA1
IgG autoantibodies
Immune complex
Mucosal immunity
Journal
Seminars in immunopathology
ISSN: 1863-2300
Titre abrégé: Semin Immunopathol
Pays: Germany
ID NLM: 101308769
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
28
06
2021
accepted:
24
07
2021
pubmed:
28
9
2021
medline:
5
4
2022
entrez:
27
9
2021
Statut:
ppublish
Résumé
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. This disease, discovered in 1968, is characterized by IgA-IgG glomerular immunodeposits with a mesangial pattern. It is thought that these immunodeposits originate from the immune complexes formed in the circulation. It is hypothesized that the pathogenesis of IgAN is driven by aberrant glycoforms of IgA1 (galactose-deficient IgA1, Gd-IgA1). Gd-IgA1, in genetically susceptible individuals, represents the initiating factor for the formation of circulating immune complexes due to its recognition by IgG autoantibodies and the subsequent formation of pathogenic IgA1-IgG immune complexes. Complement activation through alternative and/or lectin pathways is likely playing an important role in the pathogenic properties of these complexes and may further upregulate local inflammatory responses and glomerular injury.
Identifiants
pubmed: 34570260
doi: 10.1007/s00281-021-00883-8
pii: 10.1007/s00281-021-00883-8
doi:
Substances chimiques
Antigen-Antibody Complex
0
Immunoglobulin A
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
669-678Subventions
Organisme : NIAID NIH HHS
ID : R01 AI149431
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK078244
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM098539
Pays : United States
Informations de copyright
© 2021. Springer-Verlag GmbH Germany, part of Springer Nature.
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