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IL-37 Expression Is Downregulated in Lesional Psoriasis Skin

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  • Kirsten Rønholt
  • Ane Langkilde-Lauesen Nielsen
  • Claus Johansen
  • Christian Vestergaard
  • Astrid Fauerbye, Orthopaedic Research Unit, Aarhus University Hospital, Aarhus N, Denmark; Department of Clinical Medicine, Aarhus University, Aarhus N, Denmark; Department of Orthopaedic Surgery, Aarhus University Hospital, Aarhus N, Denmark.
  • ,
  • Rubèn López-Vales, Autonomous Univ Barcelona, University of Barcelona, Autonomous University of Barcelona, Corp Sanitaria Univ Parc Tauli, CIBER Enfermedades Resp, Dept Intens Care Med
  • ,
  • Charles A Dinarello, University of Colorado Denver Anschutz Medical Campus and University of Colorado Hospital, Denver, Colorado, USA.
  • ,
  • Lars Iversen

IL-37 broadly suppresses inflammation in various disease models. However, studies of the regulation and role of IL-37 in psoriasis are limited and contradictive. Using transcriptome analysis, PCR, protein determination, and immunofluorescence, we demonstrated marked downregulation of IL-37 in biopsies from human lesional psoriasis skin compared with paired samples of nonlesional skin. Immunofluorescence analysis showed that IL-37 was localized to stratum granulosum of the epidermis. TNF-α stimulation of normal human epidermal keratinocytes led to increased IL37 expression through a p38 MAPK-mediated mechanism, whereas IL-17A, IL-17C, IL-17F, and IL-22 acted suppressively. Intradermal injection with recombinant human IL-37 into imiquimod-induced psoriasis skin of C57BL/6J mice demonstrated a trend toward a protective effect, however NS. Altogether, these results demonstrate that IL-37 is downregulated in human lesional psoriasis skin. This may be a consequence of the loss of stratum granulosum, but key cytokines in the development of psoriasis also seem to contribute to this downregulation.

Original languageEnglish
Pages (from-to)754-761
Number of pages8
Publication statusPublished - Nov 2020

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