IL-1β induces expression of costimulatory molecules and cytokines but not immune feedback regulators in dendritic cells

Dendritic cells play an important role in the initiation of immune reactions. Due to their high capacity to prime T-cell responses, the activation of dendritic cells must be tightly controlled. Because Interleukin-1 beta (IL-1 beta) is a key player in autoinflammatory diseases, we compared the ability of IL-1 beta to activate human dendritic cells and induce immune-regulatory molecules versus the effects induced by pathogen-derived stimuli. Upon activation with either IL-1 beta or microbial stimuli, monocyte-derived dendritic cells showed enhanced expression of costimulatory molecules, increased secretion of chemokines and cytokines, and the ability to activate T cells. In contrast, immune-feedback molecules, including PD-L1, IL-1RA, IL-10 and SOCS1, were exclusively upregulated in response to microbial stimuli, whereas IL-1 beta treatment had no inducing effect on them. Thus, the limited capacity of IL-1 beta to induce potential feedback inhibitors may support its key etiologic role in chronic inflammation and autoinflammatory responses.