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

Cell Immunol. 2014 Nov-Dec;292(1-2):19-24. doi: 10.1016/j.cellimm.2014.08.005. Epub 2014 Aug 27.

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 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.

Keywords: Autoimmunity disease; CD4(+) T cell; Experimental autoimmune encephalomyelitis; Multiple sclerosis; Protein 4.1R.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoimmunity*
  • CD4-Positive T-Lymphocytes / immunology*
  • Cell Proliferation
  • Cells, Cultured
  • Cytoskeletal Proteins / deficiency
  • Cytoskeletal Proteins / metabolism*
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Lymphocyte Activation*
  • Membrane Proteins / deficiency
  • Membrane Proteins / metabolism*
  • Mice, Inbred C57BL
  • Mice, Knockout

Substances

  • Cytoskeletal Proteins
  • Membrane Proteins
  • protein 4.1R , mouse