Fig. 2

Aberrant production of IL-6 by the patient’s blood leukocytes. Density gradient-purified peripheral blood mononuclear cells were left unstimulated (unstim) or stimulated for 24 h with anti-CD3 + anti-CD28, lipopolysaccharide (LPS) + adenosine triphosphate (ATP), L18-muramyl dipeptide (L18-MDP), poly(deoxyadenylate–thymidylate) [poly(dA:dT)], anisomycin or the pro-inflammatory cytokines IL-1β, TNF, IFN-γ and IL-6 to respectively activate T cells, the NLRP3, NOD2, AIM2 and pyrin inflammasomes as well as cytokine signalling. Concentrations of IL-6, TNF, IL-12, IL-23, IL-1α, IL-1β, IL-18, IL-1RA, IL-17 and IFN-γ were determined by multiplex assays in the cells’ supernatants of healthy donors (black dots) and the patient with aggressive RA-like PsoA (red square). Results are expressed as mean ± standard deviation for the healthy donors (n = 5). ND; not determined