Abstract

BackgroundIloprost has been suggested to possess anti-inflammatory and immunomodulating actions and it is widely use as a vasodilatator in systemic sclerosis (SSc). In this study we evaluate the effect of iloprost on immune response in SSc patients. To this extend we enrolled 15 women affected by SSc and infused iloprost for 5 days. The effect of iloprost on T cells and monocytes was measured by flow cytometry, Real time PCR and measuring cytokines production in vivo and in vitro by ELISA.ResultsOur results demonstrate that Iloprost reduces T cell and TNF alpha production both in vivo and in vitro. It reduces T regulatory cells number, but increases their activity after immune stimulation. It increases serum IL-2 and this increase persists 28 days after the last infusion, also RANKL was increased both in vivo and in vitro. We observed no effect on IFN gamma production.ConclusionsThese results suggest that iloprost has anti-inflammatory and immunomodulating effects, reducing TNF alpha production by T cells and the number of T regulatory cells and increasing IL-2 and RANKL.

Highlights

  • Iloprost has been suggested to possess anti-inflammatory and immunomodulating actions and it is widely use as a vasodilatator in systemic sclerosis (SSc)

  • As TNF a is produced mainly by T cells and monocytes among Peripheral bood mononuclear cells (PBMCs) and it is increased in inflammation, we looked at the effect of iloprost on TNF a producing cells

  • Iloprost reduces T regs in vivo and in vitro Since altered T regulatory cells (Treg) number and activity may be important in SSc [10], we evaluated these cells as a possible iloprost target

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Summary

Introduction

Iloprost has been suggested to possess anti-inflammatory and immunomodulating actions and it is widely use as a vasodilatator in systemic sclerosis (SSc). In this study we evaluate the effect of iloprost on immune response in SSc patients. Mononuclear cells (mainly T cells) in the SSc skin infiltrates produce cytokines and growth factors responsible for the onset and progression of fibrosis and microvascular damage. The role of this immune dysfunction is not fully clear. An important role as controllers of self-reactivity [9] has recently been defined for T regulatory cells (Treg) in autoimmune disease. These cells are defined as CD4+/ CD25bright/FoxP3+. In SSc, both an increase in their absolute number and a reduction of their function have been demonstrated [10]

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