Expansion of FasL-expressing CD5+ B cells in type 1 diabetes patients

Ankit Saxena, Hideo Yagita, Thomas W. Donner, Abdel Rahim A. Hamad

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Article number402
JournalFrontiers in Immunology
Volume8
Issue numberAPR
DOIs
StatePublished - Apr 7 2017

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B-Lymphocytes
Interleukin-10
Inbred NOD Mouse
Fas Ligand Protein
Autoantibodies
Pancreas
Cell Death
Cytokines

Keywords

  • Autoimmunity
  • B cell
  • CD5
  • Fas (CD95)
  • FasL (CD178)
  • Gld
  • IL-10
  • Type 1 diabetes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Expansion of FasL-expressing CD5+ B cells in type 1 diabetes patients. / Saxena, Ankit; Yagita, Hideo; Donner, Thomas W.; Hamad, Abdel Rahim A.

In: Frontiers in Immunology, Vol. 8, No. APR, 402, 07.04.2017.

Research output: Contribution to journalArticle

Saxena, Ankit; Yagita, Hideo; Donner, Thomas W.; Hamad, Abdel Rahim A. / Expansion of FasL-expressing CD5+ B cells in type 1 diabetes patients.

In: Frontiers in Immunology, Vol. 8, No. APR, 402, 07.04.2017.

Research output: Contribution to journalArticle

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