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Decrease in the proportion of CD24hi CD38hi B cells and impairment of their regulatory capacity in type 1 diabetes

Y Wang1,2, Y Qin1, X Wang1

  • 1Department of Endocrinology, The First Affiliated Hospital with Nanjing Medical University, Nanjing Medical University, Nanjing, Jiangsu, China.

Clinical and Experimental Immunology
|December 19, 2019
PubMed

Insights

B10 cells, crucial for immune balance, are deficient in type 1 diabetes (T1D). This study reveals lower numbers and impaired function of these regulatory B cells in T1D patients, contributing to immune dysregulation in the disease.

Area of Science:

  • Immunology
  • Endocrinology
  • Autoimmunity

Background:

  • B10 cells are vital for maintaining immune homeostasis through interleukin-10 (IL-10) production.
  • Dysfunctional B10 cells are implicated in various autoimmune diseases, but their role in type 1 diabetes (T1D) remains debated.
  • This study investigates potential numerical and functional defects of B10 cells in T1D patients.

Purpose of the Study:

  • To determine the frequency and function of B10 cells in patients with type 1 diabetes (T1D).
  • To investigate the regulatory capacity of CD24hi CD38hi B cells in healthy individuals and T1D patients.
  • To explore the correlation between B10 cell levels and T cell subsets in T1D.

Main Methods:

  • Flow cytometry was used to identify and quantify B10 cells (CD24hi CD38hi B cells) in peripheral blood.
  • Functional assays assessed the regulatory capacity of B10 cells in suppressing pro-inflammatory cytokine production (IFN-γ, TNF-α, IL-17A) and promoting regulatory T cell markers (IL-4, FoxP3).
  • Statistical analyses, including Pearson's correlation, were employed to examine relationships between B10 cell frequency and T cell populations.

Main Results:

  • B10 cells were identified as a CD24hi CD38hi B cell subpopulation in human peripheral blood.
  • Healthy individuals' B10 cells exhibited regulatory capacity, suppressing IFN-γ, TNF-α, and IL-17A while promoting IL-4 and FoxP3 expression in T cells via IL-10.
  • T1D patients showed significantly lower percentages of B10 cells, reduced IL-10 production, and impaired regulatory function compared to healthy controls.
  • A negative correlation was observed between circulating B10 cell frequency and pro-inflammatory CD4+ T cells (IFN-γ+, TNF-α+), and a positive correlation with regulatory CD4+ T cells (CD25+, FoxP3+).

Conclusions:

  • Patients with T1D exhibit a deficiency in circulating CD24hi CD38hi B cells (B10 cells).
  • These B10 cell defects contribute to immune imbalance and may play a role in the pathogenesis of type 1 diabetes.
  • Restoring B10 cell function could be a potential therapeutic strategy for T1D.

Keywords:
B cellautoimmunitydiabeteshuman

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