Abstract
BackgroundChronic immune activation and hyperglycaemia are a hallmark of type 2 diabetes mellitus (T2D) while natural killer (NK) cells are involved in the pathogenesis of T2D. Dysregulated NK cell responses are associated with an increased risk of cardiovascular disease in patients living with T2D.ObjectiveTo provide a comprehensive and systematic evidence-based estimate on the levels of NK cells in patients living with T2D.ResultsThis systematic review and meta-analysis included 13 studies reporting on 491 adult patients with T2D and 1064 nondiabetic controls. The pooled effect estimates showed increased levels of NK cells in adult patients with T2D compared to controls (MD: 0.03 [− 3.20, 3.26], I2 = 97%, p < 0.00001).ConclusionOverall, the evidence presented in this systematic review shows that the changes in NK cells in patients living with T2D are still unclear and further studies are needed.
Highlights
Chronic immune activation and hyperglycaemia are a hallmark of type 2 diabetes mellitus (T2D) while natural killer (NK) cells are involved in the pathogenesis of T2D
Over 90% of patients with T2D are obese [5] and these individuals present with ectopic lipid accumulation that is associated with adipose tissue (AT) dysfunction [6]
Our group and others have provided cumulative findings showing that persistent T helper cell 1 (Th1) and Th17 cytokine levels which include tumor necrosis factor-α (TNFα), interleukin-1 (IL-1), IL-6 and IL-17 exacerbates insulin resistance which may lead to cardiovascular complications [8,9,10,11,12]
Summary
Chronic immune activation and hyperglycaemia are a hallmark of type 2 diabetes mellitus (T2D) while natural killer (NK) cells are involved in the pathogenesis of T2D. Dysregulated NK cell responses are associated with an increased risk of cardiovascular disease in patients living with T2D. More than 425 million adults are living with diabetes, with T2D accounting for approximately 90% of the cases [2]. In developing countries such as those in sub-Saharan Africa, the prevalence of T2D is expected to increase by more than two-fold in the 30 years and this coincides with an increased risk of cardiovascular disease (CVD) [3]. A dysregulation of these immune cells promotes insulin resistance [13, 14]
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