Shift in the B-cell subsets between children with type 1 diabetes and/or celiac disease.
B-cell subsets
celiac disease
children
flow cytometry
type 1 diabetes
Journal
Clinical and experimental immunology
ISSN: 1365-2249
Titre abrégé: Clin Exp Immunol
Pays: England
ID NLM: 0057202
Informations de publication
Date de publication:
22 Dec 2023
22 Dec 2023
Historique:
received:
01
11
2023
medline:
22
12
2023
pubmed:
22
12
2023
entrez:
22
12
2023
Statut:
aheadofprint
Résumé
Our purpose was to characterize the pattern of B-cell subsets in children with a combined diagnosis of type 1 diabetes (T1D) and celiac disease (C) since children with single or double diagnosis of these autoimmune diseases may differ in peripheral B-cell subset phenotype patterns. B-cells were analyzed with flow cytometry for the expression of differentiation/maturation markers to identify transitional, naive and memory B-cells. Transitional (CD24hiCD38hiCD19+) and memory Bregs (CD24hiCD27+CD19+, CD1d+CD27+CD19+, CD5+CD1d+CD19+) were classified as B-cells with regulatory capacity. Children with a combined diagnosis of T1D and C showed a pattern of diminished peripheral B-cell subsets. The B-cells compartment in children with combined diagnosis had higher percentages of memory B subsets and Bregs, including activated subsets, compared to children with either T1D or C. Children with combined diagnosis had a lower percentage of naive B-cells (CD27-CD19+; IgD+CD19+) and an increased percentage of memory B-cells (CD27+CD19+; IgD-CD19+). A similar alteration was seen among the CD39+ expressing naive and memory B cells. Memory Bregs (CD1d+CD27+CD19+) were more frequent, contrary to the lower percentage of CD5+ transitional Bregs in children with a combined diagnosis. In children with either T1D or C, the peripheral B-cell compartment was dominated by naive cells. Differences in the pattern of heterogenous peripheral B-cell repertoire subsets reflect a shifting in the B-cell compartment between children with T1D and/or C. This is an immunological challenge of impact for the pathophysiology of these autoimmune diseases.
Identifiants
pubmed: 38134245
pii: 7491212
doi: 10.1093/cei/uxad136
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the British Society for Immunology.