Interleukin-1 Receptors Are Differentially Expressed in Normal and Psoriatic T Cells

Attila Bebes,Róbert Kui,Ferenc Kovács-Sólyom,Judit Prihoda,Rolland Gyulai,Lajos Kemény

doi:10.1155/2014/472625

Attila Bebes, Róbert Kui + Show 4 more

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https://doi.org/10.1155/2014/472625

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Abstract

This study was carried out to examine the possible role of interleukin-1 (IL-1) in the functional insufficiency of regulatory T cells in psoriasis, by comparing the expression of IL-1 receptors on healthy control and psoriatic T cells. Patients with moderate-to-severe chronic plaque psoriasis and healthy volunteers, matched in age and sex, were selected for all experiments. CD4+CD25− effector and CD4+CD25+CD127low regulatory T cells were separated and used for the experiments. Expression of the mRNA of IL-1 receptors (IL-1R1, IL-1R2, and sIL-1R2) was determined by quantitative real-time RT-PCR. Cell surface IL-1 receptor expression was assessed by flow cytometry. Relative expression of the signal transmitting IL-1 receptor type 1 (IL-1R1) mRNA is higher in resting psoriatic effector and regulatory T cells, and activation induces higher IL-1R1 protein expression in psoriatic T cells than in healthy cells. Psoriatic regulatory and effector T cells express increased mRNA levels of the decoy IL-1 receptors (IL-1R2 and sIL-1R2) upon activation compared to healthy counterparts. Psoriatic T cells release slightly more sIL-1R2 into their surrounding than healthy T cells. In conclusion, changes in the expression of IL-1 receptors in psoriatic regulatory and effector T cells could contribute to the pathogenesis of psoriasis.

Highlights

Psoriasis, a common inflammatory skin disorder affecting 12% of individuals in Western societies, is caused by genetic predisposition and can be triggered or affected by various environmental provoking factors, such as mechanical stress (Koebner phenomenon), infections, emotional stress, diet, body mass index, alcohol consumption, smoking, certain drugs, and climatic effects [1,2,3]
Naıve (TN), memory (TM), naıve regulatory (TNreg), and regulatory T cell (Treg) subpopulations were identified by CD45RO and CD25/GARP labelling (Figures 1(a) and 1(b))
Similar distribution of T cell populations was found in resting normal and psoriatic samples and there was no significant difference in the cell number of control and psoriatic T cell subgroups

Summary

Introduction

A common inflammatory skin disorder affecting 12% of individuals in Western societies, is caused by genetic predisposition and can be triggered or affected by various environmental provoking factors, such as mechanical stress (Koebner phenomenon), infections, emotional stress, diet, body mass index, alcohol consumption, smoking, certain drugs, and climatic effects [1,2,3]. Published studies suggest that intralesional activated T cells produce cytokines that trigger primed basal stem cell keratinocytes to proliferate and perpetuate skin inflammation. The type 1 receptor (IL-1R1) is described as a signal transmitting receptor, triggered by both IL-1α and IL-1β ligands. The intracellular domain of IL-1R1 is responsible for initialising the inflammatory signalling processes in target cells. The type 2 IL-1 receptors (IL-1R2) are decoy receptors, as they are lacking the intracellular signal transmitting domain for mediating the IL-1 effect. IL-1R2 can be found associated with the plasma membrane and in soluble, secreted forms. Both of these receptor forms strongly bind IL-1; they are unable to initialise the IL-1 signalling pathway. Soluble IL-1R2 protein is produced by shedding from the cell surface or synthesised in a soluble form from a distinct gene

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