Höfundar:
Hildur Sigurgrímsdóttir, Jona Freysdottir, Björn Rúnar Lúðvíksson
Introduction: The immunopathogenesis of psoriasis is characterized by hyperproliferation of keratinocytes driven by skin infiltrating T cells dominated by T17/22 inflammatory pattern. Various aspects regarding the mechanisms driving this intense skin homing infiltration of pathogenic T cells remains to be elucidated. The main aim of this study was to further define the interplay of skin homing (CLA) and retention (CD103) of T cells in relation to its chemokine receptor milieu during the resolution of psoriasis.
Material and methods: T cells from peripheral blood of psoriasis patients undergoing NB-UVB treatment and healthy controls (HC) were isolated. Then chemokine receptor fingerprinting was characterized in relation to CLA and CD103 expression pattern for both CD4+ and CD8+ T cells by flow cytometry. Psoriasis severity was evaluated by Trozak and PASI.
Results: The expression of CCR4 and CCR6 was closely linked to CLA expression for CD4+ T cells in HC. In addition, CCR6 expression was higher in psoriasis patients than in HC, in T cells and in CLA+ or CD103+ subgroups. In contrast to CCR6, the expression of CXCR3 was only linked to CD103+ T cells. Expression of CCR6 and CXCR3 correlated with psoriasis severity as measured by Trozak and PASI.
Conclusion: Effector T cells with chemokine receptors closely linked to the T17/T22 inflammatory response are predominantly confined to skin homing CD4+ T cells. In addition, CCR6 and CXCR3 have a significant association with psoriasis severity suggesting that therapeutic modalities aimed at these T cell subgroups could lead to novel and improved therapeutic opportunities.