Background Dimethyl fumarate (DMF) is the active ingredient of Skilarence (TM) and Tecfidera (TM), which are used for the treatment of psoriasis and multiple sclerosis, respectively. Various immunomodulatory mechanisms of action have been identified forDMF; however, it is still unclear what effectsDMFexertsin vivoin patients with psoriasis. Objectives In this study we examined the effects ofDMF, bothin vivoandin vitro, on T cells, which play a key role in the pathogenesis of psoriasis. Methods The frequency of T-cell subsets was examined by flow cytometry in untreated patients with psoriasis or those treated withDMF. The effects ofDMFin vitroon T-cell survival, activation and proliferation, and cell-surface thiols were assessed by flow cytometry. Results In patients with psoriasis treated withDMFwe observed an increase in the frequency of T regulatory (Treg) cells and a decrease in T helper (Th)17 lineage cells and the associated cytokines interleukin-17, interleukin-22 and granulocyte-macrophage colony-stimulating factor. T cells culturedin vitrowithDMFexhibited reduced viability, and inhibition of activation and proliferation in response to stimulation due to the oxidative effects ofDMF. However, the frequency of Treg cells increased in the presence ofDMFdue to their heightened ability to resistDMF-induced oxidative stress. Conclusions DMFenhanced the ratio of Treg cells to Th17 cells in patients with psoriasis, in patients with multiple sclerosis andin vitro. Furthermore, our data suggest that this is at least in part as a result of the differential effects ofDMFon Treg cells compared with conventional T cells.

• Infection with human polyomavirus 2 (HPyV2) is common. • Reactivation of HPyV2 in immunocompromised hosts may rarely lead to a serious illness- progressive multifocal leucoencephalopathy (PML). • HPyV2 induced PML has been reported in association with systemic and biologic treatments for psoriasis , rheumatoid arthritis , haematological malignancy and multiple sclerosis . • The prevalence of HPyV2 has not been measured in a psoriasis cohort to date.

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease characterized by painful deep-seated recurrent nodules and abscesses in axillary, inguinal, and perineal areas (Jemec, 2012). It is a complex disease with an etiology including genetic variations, environmental factors, and aberrant innate and adaptive immune functions (Alikhan et al., 2009; Kelly et al., 2014; Moran et al., 2017).

Hidradenitis suppurativa (HS), is characterized by the appearance of painful subcutaneous nodules and dermal abscesses in the axillae, perineum and inframammary folds. The development of HS has been linked to factors such as cigarette smoking and obesity1. Patients with HS are more likely to have metabolic syndrome than control populations and develop early cardiovascular diseases2. Adipokines are signalling molecules secreted by adipose tissue and peripheral blood mononuclear cells. The expression of adipokines is dysregulated in obesity and cardiovascular diseases3. This article is protected by copyright. All rights reserved.