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https://www.bocsci.com/il-1-receptor-signaling-pathway.html
Overview of the IL-1 Receptor Signaling Pathway

IL-1 is a cytokine produced by activated macrophages which mediates several physiological responses to infections and injuries, including stimulation of thymocyte proliferation, B-lymphocyte maturation and proliferation, induction of acute-phase protein synthesis by hepatocytes and induction of fever. In addition to macrophages, fibroblast keratinocytes, comeal cell astrocytes, and EBV-transformed B-lymphocytes are also capable of producing IL-1. Monocyte cell lines produce IL-1 after treatment with agents such as TPA and LPS.

There are 11 members of the IL-1 family (IL-1F) of ligands including IL-1α, IL-1β, IL-1 receptor antagonist (IL-1Ra), etc. The main function of IL-1-type cytokines is to control proinflammatory reactions in response to tissue injury by pathogen-associated molecular patterns (PAMPs, such as bacterial or viral products) or damage- or danger-associated molecular patterns released from damaged cells (DAMPs, such as uric acid crystals or adenosine 5´-triphosphate). Thus, they are major mediators of innate immune reactions, and their actions are tightly balanced. The occurrence of severe multiorgan inflammation in patients with homozygous mutations or deletions of the gene encoding interleukin-1 receptor antagonist (IL-1RA) and the successful blockade of inflammatory reactions in humans by application of recombinant IL-1RA or antibodies to IL-1β have demonstrated a central role of IL-1α or IL-1β in a number of auto-inflammatory diseases. This pathway summarizes signaling of the founding members, IL-1α and IL-1β, which share only 24% amino acid sequence identity but have largely identical biological function.

Sentinel cells of the innate immune system (macrophages and monocytes) are a major source of IL-1α and IL-1β, but many other cell types, including epithelial cells, endothelial cells, and fibroblasts, can also produce IL-1α and IL-β. IL-1α is primarily membrane anchored and signals through autocrine or juxtracrine mechanisms, whereas IL-1β is secreted by an unconventional protein secretion pathway and can act in a paracrine manner or systemically. There are three major levels of control to restrict the potent proinflammatory activities of IL-1α and IL-β: (i) control of synthesis and release by the NALP3-inflammasome, a multiprotein complex that controls activation of the IL-1β–processing protease caspase-1, which was initially called interleukin-1β–converting enzyme (ICE); (ii) control of the membrane receptors; (iii) regulation of the signal transduction downstream of the activated receptors.