Liu Xin, Zhou Qingqing, Ji Zhenyu, Fu Guo, Li Yi, Zhang Xiaobei, Shi Xiaofang, Wang Ting, Kang Qiaozhen
School of Life Sciences, Zhengzhou University, 100 Science Road, Zhengzhou 450001, PR China.
Henan Academy of Medical and Pharmaceutical Sciences, Zhengzhou University, 40 University Road, Zhengzhou 450052, PR China.
Cell Immunol. 2014 Nov-Dec;292(1-2):19-24. doi: 10.1016/j.cellimm.2014.08.005. Epub 2014 Aug 27.
Immune synapse components contribute to multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) pathogenesis as they play important role in autoreactive T cell activation. Protein 4.1R, a red cell membrane cytoskeletal protein, recently was identified as an important component of immunological synapse (IS) and acted as the negative regulator of CD4(+) T cell activation. However, the pathological role of 4.1R in the MS/EAE pathogenesis is still not elucidated. In this study, we investigated the potential role of protein 4.1R in pathologic processes of EAE by using 4.1R knockout mouse model. Our results suggest that 4.1R can prevent pathogenic autoimmunity in MS/EAE progression by suppressing the CD4(+) T cell activation.
免疫突触成分在自身反应性T细胞激活中发挥重要作用，从而参与多发性硬化症（MS）和实验性自身免疫性脑脊髓炎（EAE）的发病机制。蛋白4.1R是一种红细胞膜细胞骨架蛋白，最近被确定为免疫突触（IS）的重要组成部分，并作为CD4(+) T细胞激活的负调节因子。然而，4.1R在MS/EAE发病机制中的病理作用仍未阐明。在本研究中，我们通过使用4.1R基因敲除小鼠模型，研究了蛋白4.1R在EAE病理过程中的潜在作用。我们的结果表明，4.1R可以通过抑制CD4(+) T细胞激活来预防MS/EAE进展中的致病性自身免疫。
