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- W2912489741 endingPage "54" @default.
- W2912489741 startingPage "43" @default.
- W2912489741 abstract "Immune systems have evolved to recognize and eliminate pathogens and damaged cells. In humans, it is estimated to recognize 109 epitopes and natural selection ensures that clonally expanded cells replace unstimulated cells and overall immune cell numbers remain stationary. But, with age, it faces continuous repertoire restriction and concomitant accumulation of primed cells. Changes shaping the aging immune system have bitter consequences because, as inflammatory responses gain intensity and duration, tissue-damaging immunity and inflammatory disease arise. During inflammation, the glycolytic flux cannot cope with increasing ATP demands, limiting the immune response's extent. In diabetes, higher glucose availability stretches the glycolytic limit, dysregulating proteostasis and increasing T-cell expansion. Long-term hyperglycemia exerts an accumulating effect, leading to higher inflammatory cytokine levels and increased cytotoxic mediator secretion upon infection, a phenomenon known as diabetic chronic inflammation. Here we review the etiology of diabetic chronic inflammation and its consequences on wound healing." @default.
- W2912489741 created "2019-02-21" @default.
- W2912489741 creator A5018136833 @default.
- W2912489741 creator A5043580735 @default.
- W2912489741 creator A5053810279 @default.
- W2912489741 creator A5081800814 @default.
- W2912489741 creator A5088221703 @default.
- W2912489741 date "2019-03-01" @default.
- W2912489741 modified "2023-10-18" @default.
- W2912489741 title "Immune aging in diabetes and its implications in wound healing" @default.
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