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RESEARCH PRODUCT

SAT0374 IL-36A Axis is Modulated in Patients with Primary Sjogren's Syndrome and Implicated in the Regulation of Gamma-Delta T Cells Immune Functions

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Background IL-36a is a cytokine that predominantly acts on naive CD4+ T cells and gamma-delta T cells via the IL-36 receptor. IL-36a has been recently demonstrated to be involved in human disease, such as psoriasis, by modulating innate and adaptive immune responses. Objectives In this study we aimed to investigate the expression of IL-36 axis and to assess the role of γδ T cells in patients with primary Sjogren9s syndrome (pSS). Methods Blood and minor labial salivary glands (MSG) biopsies were obtained from 35 pSS and 20 nSS patients. Serum IL-36a was assayed by ELISA. IL-36a, IL-36R, IL-36RA, IL-38, IL-22, IL-17, IL-23p19, expression in MSGs was assessed by rt-PCR and tissue IL-36a and IL-38 expression also investigated by immuno-histochemistry (IHC). ab and gδ T cells and CD68+ cells isolated from MSGs were also studied by flow cytometry and confocal microscopy analysis. Results IL-36a was significantly over-expressed in the serum and in the salivary glands of pSS. Salivary gland IL-36a mRNA expression was correlated with the expression levels of IL-17, IL-22 and IL-23p19 (r 2 =0.45, r 2 =0.66, r 2 =0.73, respectively; p + cells were confirmed to be the major source of IL-36a in minor salivary glands of pSS. gδ T cells were not significantly expanded in the salivary glands of pSS but produced more IL-17 being their percentage correlated with the focus score. Higher expression of IL-36a and IL-36R was also demonstrated in γδ T cells isolated from pSS compared to controls. Conclusions In this study we demonstrate that a significant increase in circulating and tissue levels of IL-36a occurs in pSS and provide also the first evidence of a putative role of IL-17 + /IL-36 + γδ T lymphocytes. Disclosure of Interest None declared