Pathogenesis of adult onset Stills disease

Pathogenesis of adult onset Stills disease

An unidentified infectious or environmental trigger provides a specific danger signal (e.g., pathogen-associated and damage-associated molecular patterns) that bind to toll-like receptors on macrophages and neutrophils, leading to activation of specific inflammasomes resulting in caspase activation and overproduction of IL-1β. This cytokine can further contribute to macrophage and neutrophil activation resulting in overproduction of several other proinflammatory cytokines (IL-6, IL-8, IL-17, IL-18, and TNF). Unidentified genetic factors may predispose a person to developing this cytokine storm. Alternatively, regulatory antiinflammatory mechanisms (regulatory T cells, IL-10, etc) may be defective in halting the unrestrained amplification of proinflammatory cytokines.


Sign up to receive the trending updates and tons of Health Tips

Join SeekhealthZ and never miss the latest health information