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To get more insight into the molecular mechanisms of IL-36 function, Ahn et al. [91] studied the effects of recombinant IL-36 on cultured cells. By flow cytometric analysis, they found that IL-36 induced the expression of the pro-inflammatory cytokines IL-6, IL-8, TNFα, IL-1β, and IL-12 in both BMDM and human keratinocyte cell lines. In addition, IL-36 did not induce IL-17A and T-bet expression in human Th17 cells. On the other hand, IL-36 was not able to induce IL-17A and RORC-dependent gene expression in mouse Th17 cells. They also found that IL-36 induced upregulation of surface expression of MHC class II, CD80, and CD86, all important activation markers in dendritic cells. Finally, they showed that IL-36 induced the maturation of bone marrow derived dendritic cells in vitro. Taken together, these findings indicate that IL-36 is able to modulate the activation of macrophages, dendritic cells, and keratinocytes, which are all relevant to the inflammatory response. Furthermore, through its ability to modulate the production of pro-inflammatory cytokines, IL-36 may also be involved in some of the skin inflammatory diseases in which IL-36γ is over-expressed.
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