Interleukin-36 in hidradenitis suppurativa: evidence for a distinctive proinflammatory role and a key factor in the development of an inflammatory loop

BackgroundPossible regulatory involvement of the interleukin (IL)-36 family in inflammatory diseases has been suggested. ObjectivesTo analyse the expression of IL-36, IL-36, IL-36 and the antagonistic cytokines IL-36 receptor agonist (IL-36Ra), IL-37 and IL-38 in the skin of patients with hidradenitis suppurativa (HS). MethodsSkin samples from lesional and corresponding perilesional HS skin, and from healthy controls were included in this study and analysed by quantitative real-time reverse-transcriptase polymerase chain reaction (PCR). To evaluate the PCR results of IL-36, IL-36 and IL-36, a subset of skin samples was studied by immunohistochemistry. ResultsExpression levels of IL-36, IL-36, IL-36 and IL-36Ra were all significantly higher in lesional HS skin than in healthy controls. IL-37 and IL-38 levels were significantly higher in perilesional HS skin than in healthy controls and were decreased in lesional HS skin. Limitations of the study are its descriptive nature and the small sample size. ConclusionsOur results showed a possible involvement of IL-36 cytokines in the inflammatory network of HS and a dysbalance between the agonistic and antagonistic cytokines in HS skin. What's already known about this topic? Studies have suggested an important role of the interleukin (IL)-36 family in the regulation of skin inflammation. What does this study add? Expression levels of the IL-36 cytokines and the antagonistic cytokines (IL-36Ra, IL-37 and IL-38) were significantly dysregulated in lesional and perilesional hidradenitis suppurativa (HS) skin. What is the translational message? Targeting IL-36/IL-36 receptor signalling seems to be a promising novel therapeutic approach for HS. Linked Comment:Emtestam and Sartorius. Br J Dermatol 2018; 178:591-592. Plain language summary available online Respond to this article