Adalimumab (antitumour necrosis factor-α) treatment of hidradenitis suppurativa ameliorates skin inflammation: an in situ and ex vivo study


  • Funding sources
    This study was supported financially by Abbott Immunology, Abbott Park, Chicago, IL, U.S.A.

  • Conflicts of interest
    H.H.v.d.Z. and E.P.P. were both investigators in the Abbott M10-467 phase IIB trial ( no. NTC00918255).

Hessel van der Zee.


Background  Hidradenitis suppurativa (HS) is a difficult-to-manage disease. Randomized controlled trials with antitumour necrosis factor (TNF)-α biologics have been conducted and in most studies disease activity was reduced. However, the mechanism of action in HS skin is so far unknown.

Objectives  To assess whether anti-TNF-α treatment affects in situ cytokine production and frequency of inflammatory cell populations in HS lesional skin.

Methods  Nine patients with HS, participating in a larger placebo-controlled, double-blind phase IIb clinical trial on the efficacy and safety of adalimumab in patients with moderate to severe HS (M10-467), were randomized and treated for 16 weeks. In a mechanism-of-action substudy, biopsies were obtained at fixed time points pre- and post-treatment. One part of the biopsy was cultured for 24 h for cytokine release in the culture medium, while another part was used for in situ analysis.

Results  Secretion of cytokines, including interleukin (IL)-1β, CXCL9 [monokine induced by interferon-γ (MIG)], IL-10, IL-11, B-lymphocyte chemoattractant (BLC) and IL-17A, was significantly elevated in HS. Adalimumab treatment was associated with decreased production of cytokines in HS skin, especially IL-1β, CXCL9 (MIG) and BLC. Treatment significantly reduced the number of CD11c+, CD14+ and CD68+ cells in HS lesional skin. The numbers of CD3+ and CD4+ T cells, and CD20+ and CD138+ B cells were also reduced by adalimumab treatment.

Conclusions  Adalimumab treatment inhibits important cytokines and inflammatory cell numbers in lesional HS skin, especially levels of IL-1β and numbers of inflammatory CD11c+ dendritic cells.