Clin Exp Immunol. 2023 Dec 22:uxad136. doi: 10.1093/cei/uxad136. Online ahead of print.

Andrea Tompa ^1 2, Maria Faresjö ³

Author information

¹Department of Natural Science and Biomedicine, School of Health and Welfare, Jönköping University, Jönköping, Sweden.

²Division of Diagnostics, Region Jönköping County, Jönköping, Sweden.

³Department of Life Sciences, Division of Systems and Synthetic Biology, Chalmers University of Technology, Gothenburg, Sweden.

Abstract

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.