Figure 2.

Innate immune system (i.e., macrophage) interactions with implant debris produces danger signaling (inflammasome) and pathogen (NF-κB)-associated cytokines such as IL-1β and tumor necrosis factor α (TNF-α) and increased expression of costimulatory molecules such as CD80/86, ICAM1, and HLADR where the effects on chemokine receptors such as CCR2 and CCR4 are incompletely understood. These innate responses can trigger adaptive immune responses where destructive TH1 type cytokine profiles that then require T-regulatory cells (e.g., IL-10) to control this response (courtesy of BioEngineering Solutions Inc.).