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外周血单个核细胞的激活和瘦素分泌：白细胞介素-2 和高迁移率族蛋白 B1 的新潜在作用。

Activation of Peripheral Blood Mononuclear Cells and Leptin Secretion: New Potential Role of Interleukin-2 and High Mobility Group Box (HMGB)1.

机构信息

Department of Systems Medicine, University of Rome "Tor Vergata", 00133 Rome, Italy.

Department of Medical Sciences, Fondazione Policlinico Tor Vergata, 00133 Rome, Italy.

出版信息

Int J Mol Sci. 2021 Jul 26;22(15):7988. doi: 10.3390/ijms22157988.

DOI:10.3390/ijms22157988
PMID:34360753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8347813/
Abstract

Activation of innate immunity and low-grade inflammation contributes to hyperglycemia and an onset of Type 2 Diabetes Mellitus (T2DM). Interleukin-2 (IL-2), leptin, High Mobility Group Box-1 (HMGB-1), and increased glucose concentrations are mediators of these processes also by modulating peripheral blood mononuclear cells (PBMCs) response. The aim of this study was to investigate if HMGB-1 and IL-2 turn on PBMCs and their leptin secretion. In isolated human PBMCs and their subpopulations from healthy individuals and naïve T2DM patients, leptin release, pro-inflammatory response and Toll-like Receptors (TLRs) activation was measured. After treatment with IL-2 and HMGB1, NK (Natural Killer) have the highest amount of leptin secretion, whilst NK-T have the maximal release in basal conditions. TLR4 (TAK242) and/or TLR2 (TLR2-IgA) inhibitors decreased leptin secretion after IL-2 and HMGB1 treatment. A further non-significant increase in leptin secretion was reported in PBMCs of naive T2DM patients in response to IL-2 and HMGB-1 stimulation. Finally, hyperglycemia or hyperinsulinemia might stimulate leptin secretion from PBMCs. The amount of leptin released from PBMCs after the different treatments was enough to stimulate the secretion of IL-1β from monocytes. Targeting leptin sera levels and secretion from PBMCs could represent a new therapeutic strategy to counteract metabolic diseases such as T2DM.

摘要

先天免疫和低度炎症的激活导致高血糖和 2 型糖尿病（T2DM）的发生。白细胞介素-2（IL-2）、瘦素、高迁移率族蛋白-1（HMGB-1）和葡萄糖浓度升高是这些过程的介质，也通过调节外周血单个核细胞（PBMC）反应。本研究旨在探讨 HMGB-1 和 IL-2 是否会激活 PBMC 及其瘦素分泌。在来自健康个体和初发 T2DM 患者的分离的人 PBMC 及其亚群中，测量了瘦素释放、促炎反应和 Toll 样受体（TLR）激活。在 IL-2 和 HMGB1 处理后，NK（自然杀伤）细胞具有最高量的瘦素分泌，而 NK-T 细胞在基础条件下具有最大的释放。TLR4（TAK242）和/或 TLR2（TLR2-IgA）抑制剂降低了 IL-2 和 HMGB1 处理后的瘦素分泌。在初发 T2DM 患者的 PBMC 中，IL-2 和 HMGB-1 刺激后，瘦素分泌进一步增加，但无统计学意义。最后，高血糖或高胰岛素血症可能会刺激 PBMC 中瘦素的分泌。经不同处理后从 PBMC 释放的瘦素量足以刺激单核细胞中 IL-1β 的分泌。针对 PBMCs 中的瘦素血清水平和分泌可能代表一种新的治疗策略，以对抗代谢疾病，如 T2DM。

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