Abstract

Psoriasis is a chronic, inflammatory disease affecting the skin and joints. The pathogenesis of this disease is associated with genetic, environmental and immunological factors, especially unbalanced T cell activation and improper keratinocyte differentiation. Psoriatic lesion infiltrate is composed of monocytes and T cells, and most studies have focused on the participation of T cells in the pathogenesis of this disease. Here we investigated the contribution of mononuclear phagocytes in the immunopathology observed in psoriatic patients. Significant increases in the levels of TNF, IL-1β, CXCL9, as well as the soluble forms of CD14 and CD163, were observed within the lesions of psoriatic patients compared to skin biopsies obtained from healthy individuals. Moreover, we found an association between the levels of CCL2, a monocyte attractant chemokine, and disease severity. In conclusion, our findings suggest a potential role for mononuclear phagocytes in the pathogenesis of psoriasis.

Highlights

  • Psoriasis is an autoimmune skin disorder that affects ∼2% of the world’s population, and is characterized by the exacerbated proliferation/activation of keratinocytes [1]

  • We found that mononuclear phagocytes within the skin expressed lower levels of CD14 and CD16, both in psoriatic patients and healthy subjects (HS)

  • The classical activation of mononuclear phagocytes induces the cleavage of CD14 and CD163 molecules, as well as the release of their soluble forms

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Summary

Introduction

Psoriasis is an autoimmune skin disorder that affects ∼2% of the world’s population, and is characterized by the exacerbated proliferation/activation of keratinocytes [1]. Most studies designed to elucidate the pathogenesis of psoriasis have documented the notable participation of T cells, Th1, in the development of psoriatic skin lesions [2]. In this context, IFN-γ production has been found to be increased within psoriatic lesions [2]. It was documented that IL-23, produced by dendritic cells, activates Th17 cells to produce IL-17A, IL-17F and IL-22 [4, 5] These cytokines are known to contribute to neutrophil recruitment and directly activate keratinocytes, thereby promoting hyperplasia in these cells [4,5,6]

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