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Expansion of FasL-Expressing CD5+ B Cells in Type 1 Diabetes Patients.


ABSTRACT: Fas ligand drives insulitis in the non-obese diabetic mouse model of type 1 diabetes (T1D) and negatively regulates IL-10-producing (IL-10pos) CD5+ B cells in pancreata. Relevance of these phenomena to the human disease is poorly understood. Here, using splenocytes from T1D, autoantibody (Ab+), and non-diabetic (ND) human subjects, we show that a subpopulation of CD5+ B cells that is characterized by expression of FasL (FasLhiCD5+) was significantly elevated in T1D subjects, many of whom had significantly reduced frequency of IL-10posCD5+ B cells compared to Ab+ subjects. The majority of FasLhiCD5+ B cells did not produce cytokines and were more highly resistant to activation-induced cell death than their IL-10posCD5+ counterparts. These results associate expansion of FasL-expressing CD5+ B cells with T1D and lay the groundwork for future mechanistic studies to understand specific role in disease pathogenesis.

SUBMITTER: Saxena A 

PROVIDER: S-EPMC5383713 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Expansion of FasL-Expressing CD5<sup>+</sup> B Cells in Type 1 Diabetes Patients.

Saxena Ankit A   Yagita Hideo H   Donner Thomas W TW   Hamad Abdel Rahim A ARA  

Frontiers in immunology 20170407


Fas ligand drives insulitis in the non-obese diabetic mouse model of type 1 diabetes (T1D) and negatively regulates IL-10-producing (IL-10<sup>pos</sup>) CD5<sup>+</sup> B cells in pancreata. Relevance of these phenomena to the human disease is poorly understood. Here, using splenocytes from T1D, autoantibody (Ab<sup>+</sup>), and non-diabetic (ND) human subjects, we show that a subpopulation of CD5<sup>+</sup> B cells that is characterized by expression of FasL (FasL<sup>hi</sup>CD5<sup>+</sup>  ...[more]

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