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• W2410065765 abstract "It is well known that necrotic cells are capable of promoting inflammation through releasing so-called endogenous 'danger signals' that can promote activation of macrophages, dendritic cells, and other sentinel cells of the innate immune system. However, the identity of these endogenous proinflammatory molecules, also called damage-associated molecular patterns (DAMPs), has been debated since the 'danger model' was first advanced 20 years ago. While a relatively large number of molecules have been proposed to act as DAMPs, little consensus has emerged concerning which of these represent the key activators of sterile inflammation. Here I argue that the canonical DAMPs have long been hiding in plain sight, in the form of members of the extended IL-1 cytokine family (IL-1α, IL-1β, IL-18, IL-33, IL-36α, IL-36β, and IL-36γ). The latter cytokines possess all of the characteristics expected of endogenous DAMPs and initiate inflammation in a manner strikingly similar to that utilized by the other major category of inflammatory triggers, pathogen-associated molecular patterns (PAMPs). Furthermore, many PAMPs upregulate the expression of IL-1 family DAMPs, enabling robust synergy between these distinct classes of inflammatory triggers. Thus, multiple lines of evidence now suggest that IL-1 family cytokines represent the key initiators of necrosis-initiated sterile inflammation, as well as amplifiers of inflammation in response to infection-associated tissue injury." @default.
• W2410065765 created "2016-06-24" @default.
• W2410065765 creator A5058432557 @default.
• W2410065765 date "2016-06-29" @default.
• W2410065765 modified "2023-10-15" @default.
• W2410065765 title "Cell death and inflammation: the case for IL-1 family cytokines as the canonical DAMPs of the immune system" @default.
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• W2410065765 doi "https://doi.org/10.1111/febs.13775" @default.
• W2410065765 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27273805" @default.
• W2410065765 hasPublicationYear "2016" @default.
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