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脂肪细胞 CD1d 决定肥胖中的脂肪炎症和胰岛素抵抗。

Adipocyte CD1d determines adipose inflammation and insulin resistance in obesity.

机构信息

a Department of Biological Science , Institute of Molecular Biology & Genetics, Seoul National University , Seoul , South Korea.

b Department of Medicine , University of California San Diego , San Diego , California , USA.

出版信息

Adipocyte. 2018;7(2):129-136. doi: 10.1080/21623945.2018.1440928. Epub 2018 Mar 6.

DOI:10.1080/21623945.2018.1440928
PMID:29509047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6152521/
Abstract

Obesity-induced adipose tissue inflammation is regulated by various immune cells for innate and adaptive immunity. Among adipose tissue immune cells, it has been proposed that invariant Natural Killer T (iNKT) cells play crucial roles in anti-inflammatory responses in obesity. iNKT cells recognize 'lipid' antigens loaded on CD1d of antigen presenting cells and modulate immune responses by secreting Th1 or Th2 type cytokines depending on species of lipid antigens, antigen presenting cell types, and environmental cytokine milieu. However, the regulatory mechanisms of antigen presenting cells for adipose iNKT cell stimulation have not been clearly elucidated. Recently, we have reported that CD1d expressing adipocytes could act as an antigen presenting cell for adipose iNKT cells by characterization of adipocyte-specific CD1d knockout (CD1d) mice. Upon high-fat diet (HFD) feeding, CD1d mice aggravated adipose tissue inflammation and insulin resistance compared with CD1d mice. In this commentary, we provide the additional data of adipocyte CD1d-dependent regulation of adipose iNKT cell responses as well as systemic insulin sensitivity. In addition, we discuss how the interaction between adipocytes and iNKT cells would be regulated with the progression of obesity.

摘要

肥胖引起的脂肪组织炎症受各种免疫细胞调节,用于先天和适应性免疫。在脂肪组织免疫细胞中,有人提出不变自然杀伤 T(iNKT)细胞在肥胖症中的抗炎反应中发挥关键作用。iNKT 细胞识别“脂质”抗原,这些抗原加载在抗原呈递细胞的 CD1d 上,并根据脂质抗原、抗原呈递细胞类型和环境细胞因子环境的种类,通过分泌 Th1 或 Th2 型细胞因子来调节免疫反应。然而,抗原呈递细胞对脂肪 iNKT 细胞刺激的调节机制尚不清楚。最近,我们通过对脂肪细胞特异性 CD1d 敲除(CD1d)小鼠的特征描述,报道了表达 CD1d 的脂肪细胞可以作为脂肪 iNKT 细胞的抗原呈递细胞。在高脂肪饮食(HFD)喂养下,与 CD1d 小鼠相比,CD1d 小鼠加剧了脂肪组织炎症和胰岛素抵抗。在这篇评论中,我们提供了脂肪细胞 CD1d 依赖性调节脂肪 iNKT 细胞反应以及全身胰岛素敏感性的额外数据。此外,我们还讨论了随着肥胖的进展,脂肪细胞和 iNKT 细胞之间的相互作用将如何受到调节。

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本文引用的文献

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Paracrine IL-2 Is Required for Optimal Type 2 Effector Cytokine Production.旁分泌IL-2是最佳2型效应细胞因子产生所必需的。
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Deletion of CD1d in Adipocytes Aggravates Adipose Tissue Inflammation and Insulin Resistance in Obesity.脂肪细胞中CD1d的缺失加剧肥胖状态下的脂肪组织炎症和胰岛素抵抗。
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