Protein 4.1R attenuates autoreactivity in experimental autoimmune encephalomyelitis by suppressing CD4+ T cell activation

•4.1R−/− mice was more susceptible to EAE induction.•The CD4+ T cell proliferation were increased in 4.1R−/− EAE mice.•The CD4+ T cell activation were increased in 4.1R−/− EAE mice.

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.

Graphical abstractLeukocyte infiltration and demyelination were aggravated in spinal cords in 4.1R−/− EAE mice.Figure optionsDownload full-size imageDownload as PowerPoint slide