You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Abstract
The innate immune system senses molecular patterns from invading microorganisms. Once activated, it orchestrates the inflammatory response by secreting proinflammatory cytokines, such as interleukin-1 (IL-1)–type cytokines, in particular IL-1β. IL-1 mediates the expression of a vast array of genes involved in secondary inflammation. IL-1–responsive genes coordinate all aspects of local inflammation and also attract and activate cells of the adaptive immune system at sites of infection. Moreover, the innate immune system can also sense a wide range of nonmicrobial molecular patterns that represent danger or damage signals. These signals activate the NALP3-inflammasome pathway, which plays a central role in acute and chronic sterile inflammation. Here, we describe the essential components of the NALP3-inflammasome that control processing and release of IL-1β.
