Like other members of IL-1 family, IL-36α acts through the activation of NFκB and p38 MAPK pathway.
THERM
IL-36α: a novel cytokine involved in the catabolic and inflammatory response in chondrocytes.Recent studies confer to IL-36α pro-inflammatory properties.  However, little is known about the expression and function of IL-36α in cartilage.  This study sought to analyze the expression of IL-36α in healthy and OA cartilage.  Next, we determined the effects of recombinant IL-36α on catabolism and inflammation in chondrocytes.  For completeness, part of the signaling pathway elicited by IL-36α was also explored.  IL-36α expression was evaluated by immunohistochemistry and RT-qPCR.  Expression of MMP-13, NOS2 and COX-2 was also determined in OA articular chondrocytes treated with recombinant IL-36α.  We observed a low constitutive expression of IL-36α in healthy human chondrocytes.  However, OA chondrocytes likely expressed more IL-36α than healthy chondrocytes.  In addition, immune cells infiltrated into the joint and PBMCs express higher levels of IL-36α in comparison to chondrocytes.  OA chondrocytes, treated with IL-36α, showed significant increase in the expression of MMP-13, NOS2 and COX-2.  Finally, IL-36α stimulated cells showed NFκB and p38 MAPK activated pathways.  IL-36α acts as a pro-inflammatory cytokine at cartilage level, by increasing the expression of markers of inflammation and cartilage catabolism.  Like other members of IL-1 family, IL-36α acts through the activation of NFκB and p38 MAPK pathway.
C