Cellular metabolism as a basis for immune privilege.

M Karen Newell, Elizabeth Villalobos-Menuey, Susan C Schweitzer, Mary-Ellen Harper, Robert E Camley
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Abstract

We hypothesize that the energy strategy of a cell is a key factor for determining how, or if, the immune system interacts with that cell. Cells have a limited number of metabolic states, in part, depending on the type of fuels the cell consumes. Cellular fuels include glucose (carbohydrates), lipids (fats), and proteins. We propose that the cell's ability to switch to, and efficiently use, fat for fuel confers immune privilege. Additionally, because uncoupling proteins are involved in the fat burning process and reportedly in protection from free radicals, we hypothesize that uncoupling proteins play an important role in immune privilege. Thus, changes in metabolism (caused by oxidative stresses, fuel availability, age, hormones, radiation, or drugs) will dictate and initiate changes in immune recognition and in the nature of the immune response. This has profound implications for controlling the symptoms of autoimmune diseases, for preventing graft rejection, and for targeting tumor cells for destruction.

Abstract Image

Abstract Image

Abstract Image

细胞代谢是免疫特权的基础。
我们假设,细胞的能量策略是决定免疫系统如何或是否与该细胞相互作用的关键因素。细胞的代谢状态数量有限,部分取决于细胞消耗的燃料类型。细胞燃料包括葡萄糖(碳水化合物)、脂质(脂肪)和蛋白质。我们认为,细胞转换并有效利用脂肪作为燃料的能力赋予了细胞免疫特权。此外,由于解偶联蛋白参与了脂肪燃烧过程,而且据说还能保护细胞免受自由基的伤害,因此我们假设解偶联蛋白在免疫特权中发挥了重要作用。因此,新陈代谢的变化(由氧化压力、燃料供应、年龄、激素、辐射或药物引起)将决定并引发免疫识别和免疫反应性质的变化。这对于控制自身免疫性疾病的症状、预防移植排斥反应以及靶向摧毁肿瘤细胞都有着深远的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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