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.
Department of Pediatrics, Division of Endocrinology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.
Clin Immunol. 2014 Jul;153(1):156-64. doi: 10.1016/j.clim.2014.04.006. Epub 2014 Apr 21.
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.
1 型糖尿病(T1D)是由自身反应性 T 细胞破坏胰腺中产生胰岛素的β细胞引起的。髓系来源的抑制细胞(MDSC)是最近发现的一种免疫细胞亚群,可下调 T 细胞。MDSC 数量或功能的缺陷是否可能导致 T1D 发病机制尚不清楚。我们在这里报告,MDSC 在自身免疫性糖尿病的小鼠和患者的外周血中出人意料地丰富。T1D 患者外周血 MDSC 以接触依赖性方式抑制 T 细胞增殖;然而,通过体外细胞因子诱导可增强抑制功能。这些发现表明,天然 T1D MDSC 不是最大程度的抑制性,并且促进 MDSC 抑制功能的策略可能在预防或治疗 T1D 方面有效。