The role of infiltrating immune cells in dysfunctional adipose tissue.
The role of infiltrating immune cells in dysfunctional adipose tissue.
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DOI：
10.1093/cvr/cvx108
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发表时间：
2017-07-01
影响因子：
10.8
通讯作者：
Harrison DG
中科院分区：
文献类型：
--
作者：
Guzik TJ;Skiba DS;Touyz RM;Harrison DG
脂肪组织（AT）功能障碍，其特征是失去其稳态功能，是非传染性疾病的一个标志。它的特点是慢性低度炎症，常见于肥胖、胰岛素抵抗和糖尿病等代谢性疾病。虽然传统上它是通过细胞因子或趋化因子表达增加来识别的，例如 MCP-1、RANTES、IL-6、干扰素 (IFN) γ 或 TNFα 增加，但从机制上讲，免疫细胞浸润是功能失调的 AT 的一个显着特征。这些免疫细胞包括M1和M2巨噬细胞、效应和记忆T细胞、产生IL-10的FoxP3+ T调节细胞、自然杀伤细胞和NKT细胞以及粒细胞。免疫组成因病理阶段和类型而异。浸润免疫细胞不仅产生细胞因子，还产生参与组织重塑、细胞信号传导和免疫调节的金属蛋白酶、活性氧和趋化因子。 AT 中炎症细胞的存在会影响邻近的组织和器官。在血管中，血管周围 AT 炎症会导致血管重塑、超氧化物产生、内皮功能障碍以及一氧化氮 (NO) 生物利用度丧失，从而导致血管疾病、动脉粥样硬化和斑块不稳定。功能失调的 AT 还会释放脂肪因子，如瘦素、抵抗素和内脂素，从而促进代谢功能障碍，改变全身稳态、交感神经流出、葡萄糖处理和胰岛素敏感性。抗炎和保护性脂联素减少。 AT 也可能作为自身免疫介导的炎症性疾病的重要储存库和可能的激活位点。因此，免疫细胞浸润和 AT 功能障碍之间的相互调节是一个有前途的未来治疗目标。
Adipose tissue (AT) dysfunction, characterized by loss of its homeostatic functions, is a hallmark of non-communicable diseases. It is characterized by chronic low-grade inflammation and is observed in obesity, metabolic disorders such as insulin resistance and diabetes. While classically it has been identified by increased cytokine or chemokine expression, such as increased MCP-1, RANTES, IL-6, interferon (IFN) gamma or TNFα, mechanistically, immune cell infiltration is a prominent feature of the dysfunctional AT. These immune cells include M1 and M2 macrophages, effector and memory T cells, IL-10 producing FoxP3+ T regulatory cells, natural killer and NKT cells and granulocytes. Immune composition varies, depending on the stage and the type of pathology. Infiltrating immune cells not only produce cytokines but also metalloproteinases, reactive oxygen species, and chemokines that participate in tissue remodelling, cell signalling, and regulation of immunity. The presence of inflammatory cells in AT affects adjacent tissues and organs. In blood vessels, perivascular AT inflammation leads to vascular remodelling, superoxide production, endothelial dysfunction with loss of nitric oxide (NO) bioavailability, contributing to vascular disease, atherosclerosis, and plaque instability. Dysfunctional AT also releases adipokines such as leptin, resistin, and visfatin that promote metabolic dysfunction, alter systemic homeostasis, sympathetic outflow, glucose handling, and insulin sensitivity. Anti-inflammatory and protective adiponectin is reduced. AT may also serve as an important reservoir and possible site of activation in autoimmune-mediated and inflammatory diseases. Thus, reciprocal regulation between immune cell infiltration and AT dysfunction is a promising future therapeutic target.
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影响因子：
20.1
作者：
Antonopoulos AS;Margaritis M;Verheule S;Recalde A;Sanna F;Herdman L;Psarros C;Nasrallah H;Coutinho P;Akoumianakis I;Brewer AC;Sayeed R;Krasopoulos G;Petrou M;Tarun A;Tousoulis D;Shah AM;Casadei B;Channon KM;Antoniades C
通讯作者：
Antoniades C
影响因子：
4
作者：
Akhavanpoor M;Wangler S;Gleissner CA;Korosoglou G;Katus HA;Erbel C
通讯作者：
Erbel C
影响因子：
64.8
作者：
Bettelli, E;Carrier, YJ;Kuchroo, VK
通讯作者：
Kuchroo, VK
巨噬细胞的局部扩散有助于与肥胖相关的脂肪组织炎症。
影响因子：
29
作者：
Amano SU;Cohen JL;Vangala P;Tencerova M;Nicoloro SM;Yawe JC;Shen Y;Czech MP;Aouadi M
通讯作者：
Aouadi M
影响因子：
8.3
作者：
Barhoumi, Tlili;Kasal, Daniel A.;Schiffrin, Ernesto L.
通讯作者：
Schiffrin, Ernesto L.