IL-9/IL-9R axis drives γδ T cells activation in psoriatic arthritis patients.

Cytokines such as tumor necrosis factor-α (TNF-α), IL-12, interferon-γ (IFN-γ), IL-23 and more recently IL-9, have been implicated in the initiation/maintenance of inflammation in psoriasis and psoriatic arthritis (PsA). In the present study we aimed to characterize the role of γδ T cells in peripheral blood and synovial fluid of PsA patients and to investigate their response to in vitro stimulation with antigen or cytokines (IL-9 and IL-23). γδ T cells isolated from peripheral blood mononuclear cells and synovial fluid were analyzed by flow cytometry to evaluate the phenotype and cytokine production. IL-23R and IL-9R gene expression were also evaluated by RT-PCR. PBMC, sorted γδ T cells and γδ cell lines were also stimulated in vitro with IPP, recombinant IL-9 or recombinant IL-23. Our results show an expansion of γδ T cells with a predominant effector memory phenotype in peripheral blood and synovium of untreated PsA patients, which significantly reverses after treatment with anti-TNF-α or anti-IL-12/IL-23R monoclonal antibodies (mAbs). Moreover, in PsA patients γδ T cells activation is prevalently driven by IL-9/IL-9R interaction and not only by IL-23/IL-23R. Altogether these findings indicate γδ T cells and IL-9 as new players in the pathogenesis of PsA. This article is protected by copyright. All rights reserved.

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