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.

中文翻译：

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糖尿病中的免疫老化及其对伤口愈合的影响。

免疫系统已经进化到能够识别并消除病原体和受损细胞。在人类中，估计可识别 109 个表位，自然选择可确保克隆扩增的细胞取代未受刺激的细胞，并且总体免疫细胞数量保持稳定。但是，随着年龄的增长，它面临着持续的库限制和随之而来的引发细胞的积累。塑造衰老免疫系统的变化会产生痛苦的后果，因为随着炎症反应的强度和持续时间的增加，组织损伤性免疫和炎症性疾病就会出现。在炎症期间，糖酵解通量无法应对不断增加的 ATP 需求，从而限制了免疫反应的程度。在糖尿病中，较高的葡萄糖利用率会延长糖酵解极限，导致蛋白质稳态失调并增加 T 细胞扩张。长期高血糖会产生累积效应，导致感染后炎症细胞因子水平升高和细胞毒性介质分泌增加，这种现象称为糖尿病慢性炎症。在这里，我们回顾糖尿病慢性炎症的病因及其对伤口愈合的影响。