Myeloid-derived suppressor cells are increased in frequency but not maximally suppressive in peripheral blood of Type 1 Diabetes Mellitus patients.
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.
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.
Fatima
F
Whitfield-Larry
Department of Pediatrics, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.
Jamie
J
Felton
Department of Medicine, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.
John
J
Buse
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: masu@email.unc.edu.
Maureen A
MA
Su
D000293:Adolescent; D000328:Adult; D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism; D016022:Case-Control Studies; D002450:Cell Communication / Q000276:immunology; D002648:Child; D016207:Cytokines / Q000494:pharmacology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D007958:Leukocyte Count; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D008875:Middle Aged; D022423:Myeloid Cells / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D063268:Sialic Acid Binding Ig-like Lectin 3 / Q000378:metabolism; D013154:Spleen / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D055815:Young Adult
D039481:CD11b Antigen; D016207:Cytokines; D063268:Sialic Acid Binding Ig-like Lectin 3
Myeloid-derived suppressor cells; T cell suppression; Type 1 diabetes mellitus