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Myeloid-derived suppressor cells are increased in frequency but not maximally suppressive in peripheral blood of Type 1 Diabetes Mellitus patients.

Authors
  • Whitfield-Larry, Fatima1
  • Felton, Jamie2
  • Buse, John3
  • Su, Maureen A4
  • 1 Department of Pediatrics, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
  • 2 Department of Pediatrics, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.
  • 3 Department of Medicine, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.
  • 4 Department of Pediatrics, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address: [email protected]
Type
Published Article
Journal
Clinical Immunology
Publisher
Elsevier
Publication Date
July 2014
Volume
153
Issue
1
Pages
156–164
Identifiers
DOI: 10.1016/j.clim.2014.04.006
PMID: 24769355
Source
Medline
Keywords
License
Unknown

Abstract

Type 1 Diabetes Mellitus (T1D) results from the destruction of insulin-producing beta cells in the pancreas by autoreactive T cells. Myeloid derived suppressor cells (MDSCs) are a recently identified immune cell subset that down-regulate T cells. Whether defects in MDSC numbers or function may contribute to T1D pathogenesis is not known. We report here that MDSCs are unexpectedly enriched in peripheral blood of both mice and patients with autoimmune diabetes. Peripheral blood MDSCs from T1D patients suppressed T cell proliferation in a contact-dependent manner; however, suppressive function could be enhanced with in vitro cytokine induction. These findings suggest that native T1D MDSCs are not maximally suppressive and that strategies to promote MDSC suppressive function may be effective in preventing or treating T1D.

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