Abstract
Type 1 diabetes (T1D) affects millions of people worldwide and is the prevalent form of all pediatric diabetes diagnoses. T1D is recognized to have an autoimmune etiology, since failure in specific self-tolerance mechanisms triggers immune reactions towards self-antigens and causes disease onset. Among all the different immunocytes involved in T1D etiopathogenesis, a relevant role of natural killer cells (NKs) is currently emerging. NKs represent the interface between innate and adaptive immunity; they intervene in the defense against infections and present, at the same time, typical features of the adaptive immune cells, such as expansion and generation of memory cells. Several recent studies, performed both in animal models and in human diabetic patients, revealed aberrations in NK cell frequency and functionality in the peripheral blood and in damaged tissues, suggesting their possible redirection towards affected tissues. NKs oscillate from a quiescent to an activated state through a delicate balance of activating and inhibitory signals transduced via surface receptors. Further accurate investigations are needed to elucidate the exact role of NKs in T1D, in order to develop novel immune-based therapies able to reduce the disease risk or delay its onset.
Highlights
Diabetes mellitus (DM) is a chronic metabolic disorder caused by either impaired insulin secretion or insulin action, or both [1]
The three broad categories of DM are titled as Type 1 (T1D), Type 2 diabetes (T2D) and gestational diabetes mellitus (GDM) [2]
CD56dim accounts for about 90% of the total natural killer cells (NKs) in peripheral blood, and it is a mature subpopulation with a high killer cell immunoglobulin-like receptor (KIR) expression; they are deeply involved in cytotoxicity responses and synthesize little amounts of interferon γ (IFN-γ)
Summary
Diabetes mellitus (DM) is a chronic metabolic disorder caused by either impaired insulin secretion or insulin action, or both [1]. Experimental studies highlight the role of resident islet macrophages in diabetogenesis for their interaction with β cells and blood components [26] They play distinct functions both contributing to the development and progression of disease by presenting autoantigens to naïve T cells in the draining lymph nodes and as effector cells once islet inflammation is established [27]. They elicit diabetogenic effects by generating nitric oxide (NO) and by producing inflammatory cytokines such as IL-1β and TNF. We present perspectives derived from our recent insights that open pathways for future research and translational applications
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