2型糖尿病
促炎细胞因子
免疫系统
发病机制
医学
脂肪组织
细胞因子
内科学
内分泌学
单核细胞
巨噬细胞
免疫学
糖尿病
炎症
生物
体外
生物化学
作者
Xiaojiang Dai,Junfang Zhan,Todd A. Demmy,Fred B. Poordad,Paulette L. Fauceglia,Hongbin Zhang,Liangping Wu
标识
DOI:10.1177/0394632015598848
摘要
Type 2 diabetes (T2D) is a chronic metabolic disorder, which was also found to involve a series of inflammatory disorders, including accumulation of macrophages and T cells in the adipose tissue, increased proinflammatory cytokine production, shifting of macrophage composition toward M1-type, and skewing of peripheral blood T cells toward IL-17 productions. However, these studies were primarily conducted in obese mouse models and/or human subjects with higher BMI, and may not reflect the role of the immune system in non-obese T2D pathogenesis. Here, we examined T cell and monocyte cytokine expression and function in both non-obese and obese T2D patients. We found that IFN-g production by circulating T cells were increased in both non-obese and obese T2D subjects, while IL-17 is only upregulated in obese T2D subjects. Also, circulating monocytes from obese T2D subjects had significantly higher IL-6 production than their counterparts in non-obese T2D subjects. Moreover, monocytes from non-obese T2D subjects could support IFN-g but not IL-17 production in vitro, while that from obese T2D subjects supported both IFN-g and IL-17 production. Together, our results revealed that the role immune system plays in T2D pathogenesis is more complicated than previously thought, and is affected by the person's BMI.
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