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首页> 外文期刊>Current Immunology Reviews >CD24 in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis: Targeting Redundancy for Immunotherapy?
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CD24 in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis: Targeting Redundancy for Immunotherapy?

机译：实验性自身免疫性脑脊髓炎和多发性硬化中的CD24：针对免疫疗法的冗余性？

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摘要

An interesting puzzle in the field of T cell costimulation is the apparent redundancy of costimulatory molecules for T cell activation. Our analysis over the last decade of CD24 may shed some light on the issue. CD24 was first identified as a costimulatory molecule for T cell activation over 12 years ago when we used activated B cells as antigen-presenting cells. Subsequent studies using mice with a targeted mutation of CD24 revealed that CD24 has an overlapping function with CD28 although it is dispensable for T cell activation in the lymphoid organs. Surprisingly, mice with a targeted mutation of CD24 are completely resistant to experimental autoimmune encephalomyelitis (EAE). Both T cells and non-T host cells must express CD24 in order to develop EAE. CD24 expression on non-T cells controls the local expansion of the pathogenic T cells in the central nervous system (CNS), while T cell expression of the CD24 gene is essential for homeostatic proliferation of T cells in a lymphopenic environment. The significance of CD24 in human autoimmune diseases is highlighted by the discovery that CD24 polymorphism is a genetic modifier for the risk and progression of multiple sclerosis. Thus, a costimulatory molecule redundant in the lymphoid organ can be essential for immune response in target organs. This type of costimulatory molecules is an ideal target for immunotherapy of the autoimmune diseases.
机译：T细胞共刺激领域中一个有趣的难题是用于T细胞活化的共刺激分子的明显冗余。我们对CD24过去十年的分析可能为这个问题提供了一些启示。 12年前，当我们使用活化的B细胞作为抗原呈递细胞时，CD24被首次鉴定为T细胞活化的共刺激分子。随后使用具有CD24靶向突变的小鼠进行的研究表明，CD24与CD28具有重叠功能，尽管它对于淋巴器官中的T细胞活化是必不可少的。出人意料的是，具有CD24靶向突变的小鼠对实验性自身免疫性脑脊髓炎（EAE）完全耐药。为了发展EAE，T细胞和非T宿主细胞都必须表达CD24。非T细胞上的CD24表达控制中枢神经系统（CNS）中致病性T细胞的局部扩增，而CD24基因的T细胞表达对于淋巴细胞减少环境中T细胞的稳态增殖至关重要。 CD24多态性是多发性硬化症风险和进展的遗传修饰因子，这一发现突显了CD24在人类自身免疫性疾病中的重要性。因此，淋巴器官中多余的共刺激分子对于靶器官中的免疫反应可能是必不可少的。这种类型的共刺激分子是自身免疫疾病的免疫疗法的理想靶标。

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