Protein 4.1R attenuates autoreactivity in experimental autoimmune encephalomyelitis by suppressing CD4+ T cell activation
作者： Xin Liu , Qingqing Zhou , Zhenyu Ji , Guo Fu , Yi Li
DOI: 10.1016/J.CELLIMM.2014.08.005
关键词: T cell 、 Experimental autoimmune encephalomyelitis 、 Knockout mouse 、 Biology 、 Immunology 、 Autoimmunity 、 Cytoskeleton 、 Multiple sclerosis 、 Pathogenesis 、 Immunological synapse
摘要: Abstract 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 membrane cytoskeletal protein, recently was identified an component of immunological (IS) acted the negative regulator CD4+ However, pathological 4.1R MS/EAE is still not elucidated. In this study, we investigated potential protein pathologic processes EAE by using knockout mouse model. Our results suggest that can prevent pathogenic autoimmunity progression suppressing
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