Dysregulated Antibody, Natural Killer Cell and Immune Mediator Profiles in Autoimmune Thyroid Diseases.
anti-thyroid peroxidase antibody (TPOAb)
antibody-dependent cell-mediated cytotoxicity (ADCC)
apoptosis
autoimmune thyroid diseases (AITD)
genetic variants
multi-omic
Journal
Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052
Informations de publication
Date de publication:
09 03 2020
09 03 2020
Historique:
received:
12
02
2020
revised:
04
03
2020
accepted:
05
03
2020
entrez:
19
3
2020
pubmed:
19
3
2020
medline:
17
3
2021
Statut:
epublish
Résumé
The pathogenesis of autoimmune thyroid diseases (AITD) is poorly understood and the association between different immune features and the germline variants involved in AITD are yet unclear. We previously observed systemic depletion of IgG core fucosylation and antennary α1,2 fucosylation in peripheral blood mononuclear cells in AITD, correlated with anti-thyroid peroxidase antibody (TPOAb) levels. Fucose depletion is known to potentiate strong antibody-mediated NK cell activation and enhanced target antigen-expressing cell killing. In autoimmunity, this may translate to autoantibody-mediated immune cell recruitment and attack of self-antigen expressing normal tissues. Hence, we investigated the crosstalk between immune cell traits, secreted proteins, genetic variants and the glycosylation patterns of serum IgG, in a multi-omic and cross-sectional study of 622 individuals from the TwinsUK cohort, 172 of whom were diagnosed with AITD. We observed associations between two genetic variants (rs505922 and rs687621), AITD status, the secretion of Desmoglein-2 protein, and the profile of two IgG N-glycan traits in AITD, but further studies need to be performed to better understand their crosstalk in AITD. On the other side, enhanced afucosylated IgG was positively associated with activatory CD335
Identifiants
pubmed: 32182948
pii: cells9030665
doi: 10.3390/cells9030665
pmc: PMC7140647
pii:
doi:
Substances chimiques
Autoantibodies
0
thyroid microsomal antibodies
0
Fucose
28RYY2IV3F
Iodide Peroxidase
EC 1.11.1.8
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Medical Research Council
ID : MR/L011859/1
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : British Heart Foundation
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/K006584/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/P021573/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_17214
Pays : United Kingdom
Organisme : Alzheimer's Society
ID : 171
Pays : United Kingdom
Organisme : Arthritis Research UK
Pays : United Kingdom
Organisme : Medical Research Council
ID : PG 1087407
Pays : United Kingdom
Organisme : Chief Scientist Office
Pays : United Kingdom
Organisme : Cancer Research UK
Pays : United Kingdom
Organisme : Department of Health
ID : 05/40/04
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_13041
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/L023091/1
Pays : United Kingdom
Organisme : Department of Health
ID : RP-PG-0407-10314
Pays : United Kingdom
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