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Function cytokine that presents both nuclear and extracellular functions. Extracellular IL-1 is now recognized to be an important player in sterile inflammatory diseases and cancer.117?19 IL-1 expression and intracellular function IL-1 precursor (pIL-1) is constitutively expressed in most resting nonhematopoietic cells, such as epithelial cells lining the gastrointestinal tract, liver, kidney and
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Is inhibited by the cytosolic expression of IL-1 receptor-2 (IL-1R2) that binds to pIL-1 and thereby prevents its interaction with calpain and its subsequent secretion (4). However, active caspase-1 cleaves IL-1R2 and thereby enables pIL-1 processing. pIL-1 can also be passively released from damaged cells and, similar to mature IL-1, interacts with IL-1 receptor-1 (IL-1R1) (5). In addition to bei
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Ng inflammation through the recruitment of macrophages.151,156 This mechanism is confirmed by the IL-1 dependency of IL-1 secretion following inflammasome activation.137 During brain ischemia, activated platelets present in the brain vasculature were shown to release pIL-1 and thereby stimulate endothelial cells to secrete the chemokine CXCL1 and express the endothelial surface adhesion proteins V
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Is inhibited by the cytosolic expression of IL-1 receptor-2 (IL-1R2) that binds to pIL-1 and thereby prevents its interaction with calpain and its subsequent secretion (4). However, active caspase-1 cleaves IL-1R2 and thereby enables pIL-1 processing. pIL-1 can also be passively released from damaged cells and, similar to mature IL-1, interacts with IL-1 receptor-1 (IL-1R1) (5). In addition to bei
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Ar ImmunologyDual-function alarmins in the heart of inflammation and disease D Bertheloot and E Latzstage tumor growth or blood vessel clogging. Interestingly, pIL-1 expression was shown to be increased before epithelial cell necrosis in a hypoxia-induced factor (HIF)-1a- and HIF-2a-dependent manner.154 The release of IL-1 promotes chemokine secretion and neutrophil infiltration. Moreover, extrace
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Dependent secretion mechanism.139,140 Further differentiating itself from IL-1 and HMGB1, IL-1 activation and secretion is inhibited by autophagy. Indeed, in the context of Mycobacterium tuberculosis infection, ATG5-dependent autophagy was shown to block both the calpain-dependent activation of IL-1 and its secretion, thereby limiting lung inflammation and tissue damage.141 Another regulatory mech
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Dependent secretion mechanism.139,140 Further differentiating itself from IL-1 and HMGB1, IL-1 activation and secretion is inhibited by autophagy. Indeed, in the context of Mycobacterium tuberculosis infection, ATG5-dependent autophagy was shown to block both the calpain-dependent activation of IL-1 and its secretion, thereby limiting lung inflammation and tissue damage.141 Another regulatory mech
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Streammitogen-activated protein kinase (MAPK) signaling and NFB activation (Figure 2).149,150 Thus, IL-1 activates neighboring fibroblasts or epithelial cells, further triggering the release of chemokines that leads immune cells, preferentially neutrophils,151 to infiltrate and enhance local inflammation. IL-1 in sterile inflammation: from acute to chronic disease As previously mentioned, pIL-1 is