摘要：SummaryRegulatory T cells (Treg) prevent the migration of effector T cells toward sites of inflammation, thereby limiting disease progression. We investigated this aspect of Treg function using psoriatic arthritis (PsA) as an exemplar of chronic inflammation. Patients with PsA had an increased Th17:Treg ratio which was reversed by anti-tumor necrosis factor (TNF) therapy. Utilizing anin vitromigration assay, Treg from patients with PsA treated with conventional therapy paradoxically boosted CCR6+effector T-cell (a surrogate for Th17) migration toward CCL20. In contrast, Treg from patients with PsA treated with anti-TNF suppressed CCL20-driven effector T-cell migration. The boosting effect of TNF blockade upon Treg suppression of migration was accompanied by increased effector T-cell CCL20 production and enhanced interaction between Treg and effector T cells. This study provides mechanistic insight into Treg modulation of effector T-cell migration in patients with chronic inflammation and how this can be targeted by therapy.Graphical abstractDisplay OmittedHighlights•A transwell assay can measure Treg control of effector T-cell migration•Treg enhanced effector T-cell migration toward CCL20 in psoriatic arthritis•Anti-TNF induced Treg suppressed effector T-cell migration in psoriatic arthritis•Increased Th17:Treg ratio was reversed by anti-TNF in psoriatic arthritisBiological sciences; Immunology; Immune system disorder
