Das Undurti N
UND Life Sciences, 2221 NW 5th St, Battle Ground, WA, 98604, USA.
Department of Biotechnology, Indian Institute of Technology-Hyderabad, Sangareddy, Telangana, 502284, India.
Eur J Clin Nutr. 2023 Jun;77(6):637-651. doi: 10.1038/s41430-022-01173-8. Epub 2022 Jun 14.
Autoimmune diseases are driven by T17 cells that secrete pro-inflammatory cytokines, especially IL-17. Under normal physiological conditions, autoreactive T cells are suppressed by TGF-β and IL-10 secreted by microglia and dendritic cells. When this balance is upset due to injury, infection and other causes, leukocyte recruitment and macrophage activation occurs resulting in secretion of pro-inflammatory IL-6, TNF-α, IL-17 and PGE2, LTs (leukotrienes) accompanied by a deficiency of anti-inflammatory LXA4, resolvins, protecting, and maresins. PGE2 facilitates T1 cell differentiation and promotes immune-mediated inflammation through T17 expansion. There is evidence to suggest that autoimmune diseases can be suppressed by anti-inflammatory bioactive lipids LXA4, resolvins, protecting, and maresins. These results imply that systemic and/or local application of LXA4, resolvins, protecting, and maresins and administration of their precursors AA/EPA/DHA could form a potential therapeutic approach in the prevention and treatment of autoimmune diseases.
自身免疫性疾病由分泌促炎细胞因子(尤其是白细胞介素-17)的T17细胞驱动。在正常生理条件下,自身反应性T细胞受到小胶质细胞和树突状细胞分泌的转化生长因子-β和白细胞介素-10的抑制。当由于损伤、感染和其他原因导致这种平衡被打破时,白细胞募集和巨噬细胞激活就会发生,导致促炎白细胞介素-6、肿瘤坏死因子-α、白细胞介素-17和前列腺素E2、白三烯分泌,同时抗炎性脂氧素A4、消退素、保护素和促消退介质缺乏。前列腺素E2促进T1细胞分化,并通过T17细胞扩增促进免疫介导的炎症。有证据表明,抗炎生物活性脂质脂氧素A4、消退素、保护素和促消退介质可抑制自身免疫性疾病。这些结果表明,全身和/或局部应用脂氧素A4、消退素、保护素和促消退介质以及给予它们的前体花生四烯酸/二十碳五烯酸/二十二碳六烯酸可能构成预防和治疗自身免疫性疾病的潜在治疗方法。