Abstract

The pathogenesis of Psoriatic Arthritis (PsA) remains poorly understood. The underlying chronic inflammatory immune response is thought to be triggered by unknown environmental factors and might arise due to an impaired (innate) immune function by Dendritic Cells (DCs) [1]. Anti-inflammatory CD163+ type 2 macrophages (mf-2) are thought to have important functions in restoring immune homeostasis during an inflammatory response. Mf-2 are present in PsA synovium at high numbers. Why the immune response in PsA goes awry, despite the presence of these mf-2, is still largely undetermined.

Highlights

  • The pathogenesis of Psoriatic Arthritis (PsA) remains poorly understood

  • CCR5 was significantly increased on mf-2 from PsA patients compared to healthy controls while the expression of CCR1, TLR2, TLR4 and CD14 was unaltered

  • Further research revealed that PsA mf-2 secreted more

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Summary

Introduction

The pathogenesis of Psoriatic Arthritis (PsA) remains poorly understood. The underlying chronic inflammatory immune response is thought to be triggered by unknown environmental factors and might arise due to an impaired (innate) immune function by Dendritic Cells (DCs) [1]. Anti-inflammatory CD163+ type 2 macrophages (mf-2) are thought to have important functions in restoring immune homeostasis during an inflammatory response. Mf-2 are present in PsA synovium at high numbers. Why the immune response in PsA goes awry, despite the presence of these mf-2, is still largely undetermined

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