YIM-P44. Reduced expression of cd73 on jia synovial lymphocytes is related to cell proliferation

Sophie Botta Gordon-Smith,Robin Callard,Simona Ursu,Lucy Wedderburn

doi:10.1186/1546-0096-12-s1-y4

Sophie Botta Gordon-Smith, Robin Callard + Show 2 more

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https://doi.org/10.1186/1546-0096-12-s1-y4

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Abstract

The nucleoside adenosine exerts regulatory functions prompting T cell anergy and preventing release of inflammatory cytokines. The main source of extracellular adenosine is AMP dephosphorylated by CD73. The resulting product can be taken up by the cell or further metabolized by ADA (Adenosine deaminase) expressed extracellularly when bound to the membrane via coupling to CD26 protein, a surrogate marker for ADA expression. We have shown that CD73 expression and its AMPase activity are reduced on JIA (juvenile idiopathic arthritis) SFMC (synovial fluid mononuclear cells), particularly on CD8+ T cells and CD19+ B cells; we hypothesise that this may lead to a defect in generation of anti inflammatory adenosine in JIA.

Highlights

The nucleoside adenosine exerts regulatory functions prompting T cell anergy and preventing release of inflammatory cytokines
We have shown that CD73 expression and its AMPase activity are reduced on JIA SFMC, on CD8+ T cells and CD19+ B cells; we hypothesise that this may lead to a defect in generation of anti inflammatory adenosine in JIA
Higher levels of CD73 protein were found in culture supernatants of TCR stimulated cells (53.8 ng/ml) than that of cells cultured in medium alone (29.9 ng/ml, p=0.03) suggesting that TCR stimulation leads to shedding of CD73 protein

Summary

Introduction

The nucleoside adenosine exerts regulatory functions prompting T cell anergy and preventing release of inflammatory cytokines. The main source of extracellular adenosine is AMP dephosphorylated by CD73. The resulting product can be taken up by the cell or further metabolized by ADA (Adenosine deaminase) expressed extracellularly when bound to the membrane via coupling to CD26 protein, a surrogate marker for ADA expression. We have shown that CD73 expression and its AMPase activity are reduced on JIA (juvenile idiopathic arthritis) SFMC (synovial fluid mononuclear cells), on CD8+ T cells and CD19+ B cells; we hypothesise that this may lead to a defect in generation of anti inflammatory adenosine in JIA

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