Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disease leading to immune-mediated destruction of pancreatic beta cells, resulting in the need for insulin therapy. The incidence of T1D is increasing worldwide, thus prompting researchers to investigate novel immunomodulatory strategies to halt autoimmunity and modify disease progression. T1D is considered as a multifactorial disease, in which genetic predisposition and environmental factors interact to promote the triggering of autoimmune responses against beta cells. Over the last decades, it has become clear that vitamin D exerts anti-inflammatory and immunomodulatory effects, apart from its well-established role in the regulation of calcium homeostasis and bone metabolism. Importantly, the global incidence of vitamin D deficiency is also dramatically increasing and epidemiologic evidence suggests an involvement of vitamin D deficiency in T1D pathogenesis. Polymorphisms in genes critical for vitamin D metabolism have also been shown to modulate the risk of T1D. Moreover, several studies have investigated the role of vitamin D (in different doses and formulations) as a potential adjuvant immunomodulatory therapy in patients with new-onset and established T1D. This review aims to present the current knowledge on the immunomodulatory effects of vitamin D and summarize the clinical interventional studies investigating its use for prevention or treatment of T1D.
Highlights
Pathogenesis and Natural History of Type 1 DiabetesType 1 diabetes (T1D) is an organ-specific chronic autoimmune disease leading to immunemediated destruction of insulin-secreting beta cells within the pancreatic islets, resulting in lifelong dependence on exogenous insulin [1,2]
This review aims to describe the immunomodulatory effects of vitamin D and to provide an overview of the studies evaluating the impact of vitamin D status, vitamin
C-peptide in patients with new-onset T1D, potentially resulting in a greater preservation of residual beta-cell mass and function. These findings suggest that SNPs in genes critical for synthesis, transport, and action of vitamin D may affect the risk of T1D development
Summary
Type 1 diabetes (T1D) is an organ-specific chronic autoimmune disease leading to immunemediated destruction of insulin-secreting beta cells within the pancreatic islets, resulting in lifelong dependence on exogenous insulin [1,2]. Nutrients 2019, 11, 2185 histological hallmark of T1D; it consists of the infiltration of pancreatic islets by macrophages, T helper cells (CD4+ or Th cells), and cytotoxic T cells (CD8+), resulting in the destruction of beta cells [3]. CD4+ T cells mediate the triggering of the autoimmune process and promote recruitment and activation of CD8+ T cells within the pancreatic islets. Autoreactive CD8+ T cells recognize major histocompatibility complex (MHC) class I-restricted islet autoantigens on the beta-cell surface and exert their cytotoxic effects through several effector mediators, including Th1 cytokines (e.g., TNF-α, IFN-γ) [4,5]. Defects in the ability of regulatory T cells (Tregs) to suppress activity and proliferation of CD4+ and CD8+ T cells have been reported [7,8,9]
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