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【medical-news】干扰素r和Th1细胞因子在肥胖患者获
Adipose tissue (AT) can accumulate macrophages and secrete several inflammatory mediators. Despite its pivotal role in the progression of chronic inflammatory processes such as atherosclerosis, the adaptive role of immunity in obesity remains poorly explored. Visceral AT of diet-induced obese C57BL/6 mice had higher numbers of both CD4+ and CD8+ T cells than lean controls, monitored by flow cytometry. When stimulated in vitro, T cells from obese AT produced more interferon (IFN) than those from controls. AT from obese animals also had more cells expressing I-Ab, a mouse class II histocompatibility marker implicated in antigen presentation, as determined by immunostaining. Differentiated 3T3-L1 cells stimulated with recombinant IFN or T-helper 1–derived supernatant produced several chemokines and their mRNAs. Obese IFN-deficient animals had significantly reduced AT expression of mRNA-encoding inflammatory genes such as tumor necrosis factor- and monocyte chemoattractant protein-1, decreased AT inflammatory cell accumulation, and better glucose tolerance than control animals consuming the same diet. Obese mice doubly deficient for IFN receptor and apolipoprotein (Apo)E on a mixed 129SvEv/C57BL/6 (129/B6) genetic background, despite exhibiting similar AT mRNA levels of tumor necrosis factor- and monocyte chemoattractant protein-1 as 129/B6-ApoE–/– controls, had decreased expression of important T cell–related genes, such as IFN-inducible protein-10 and I-Ab, and lower plasma triglycerides and glucose. These results indicate a role for T cells and IFN, a prototypical T-helper 1 cytokine, in regulation of the inflammatory response that accompanies obesity.
Key Words: inflammation • obesity • adipose tissue • T cell • IFN Interferon-r, a Th1 Cytokine, Regulates Fat Inflammation：A Role for Adaptive Immunity in Obesity
干扰素r和Th1细胞因子在肥胖患者获得性免疫中的角色 干扰素r和Th1细胞因子在肥胖患者获得性免疫中的角色 [/color]
脂肪组织（AT）可以积累巨噬细胞和分泌一些炎症介质。尽管其在慢性炎症如动脉粥样硬化进展中有重要作用，但在肥胖患者中的适应性角色却研究的很少。用流式细胞仪检测，饮食诱导的肥胖C57BL/6 大鼠内脏脂肪组织比瘦的对比组有更多的CD4+和CD8+ T细胞表达。体外刺激时，与对照组相比，肥胖脂肪组织的T细胞产生更多的干扰素（IFN）。肥胖动物的脂肪组织也有更多的细胞表达I-Ab，用免疫染色检测II类大鼠在抗原递呈中的组织相容性标志物。不同的3T3-L1 细胞用联合干扰素和Th1细胞刺激产生一些化学增活素和mRNAs。缺乏IFN的肥胖者明显减少mRNA编码炎症基因比如肿瘤坏死因子和 MCP-1的脂肪组织表达，也减少脂肪组织炎症细胞的堆积和与相同饮食的动物相比有更高的葡萄糖耐量。在混合的129SvEv/C57BL/6 (129/B6)基因背景下，IFN受体和载脂蛋白(Apo)E缺乏两倍的肥胖大鼠尽管在肿瘤坏死因子和MCP-1表达相似的脂肪组织mRNA水平，但却降低重要的T细胞相关基因如IFN介导的蛋白-10和I-Ab的表达，同时减少血浆甘油三酯和葡萄糖。这些结果表明T细胞，IFN和原型Th1细胞因子在肥胖患者中伴发的炎症反应中的调节作用。
关键词 炎症 肥胖 脂肪组织 T细胞 干扰素
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作者:admin@医学,生命科学 2010-12-13 17:11
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