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Drum0suede

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O moderate its negative effects will be crucial for the efficient treatment of many patients. INTERLEUKIN-1a The IL-1 family of proteins contains 11 members. The beststudied family members are IL-1 and IL-1. Both are highly similar in structure and bind to the same cell membrane receptor, IL-1R. Interestingly, IL-1 receptor antagonist (IL-1Ra) is a naturally expressed member of the IL-1 family tha
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Systemic sclerosis fibroblasts, pIL-1 translocation was shown to depend on binding to HS1associated protein X-1 (HAX-1) and induce the expression of IL-6 and pro-collagen (Figure 2).129 Interestingly, HAX-1 was also found to interact with the cleaved IL-1 N-terminal domain.130 Together, these studies suggest that the nuclear function of pIL-1 is predominantly dependent on its N-terminal domain. Up
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Ling pIL-1 processing by calpain and the release of mature IL-1. However, Gross et al.137 showed that caspase-1 dependency for IL-1 secretion can differ depending on the stimulus and the targeted inflammasomes and does not seem to require the protease activity of caspase-1. IL-1 secretion may therefore rely on redundant parallel pathways. In fact, elevated intracellular Ca2+ triggers IL-1 secretio
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Systemic sclerosis fibroblasts, pIL-1 translocation was shown to depend on binding to HS1associated protein X-1 (HAX-1) and induce the expression of IL-6 and pro-collagen (Figure 2).129 Interestingly, HAX-1 was also found to interact with the cleaved IL-1 N-terminal domain.130 Together, these studies suggest that the nuclear function of pIL-1 is predominantly dependent on its N-terminal domain. Up
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Released from necrotic cells and subsequently activates IL-1R1 present at the surface of mesothelial cells. This was proposed to be the prime event inducing neutrophil infiltration and peritoneal inflammation rather than the HMGB1 pathway.152,153 This proinflammatory role of IL-1 was recently confirmed in a mouse model of acute colon inflammation (dextran sodium sulfate-induced colitis), where epi
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Icated in platelet activation.116 Hence, in atherosclerotic plaques, HMGB1 sensing by platelets, endothelial cells and SMCs promotes the migration and adhesion of immune cells, thereby fostering plaque formation and growth. For the past two decades, HMGB1 commanded the attention of many groups because of its central role in signaling infection and cellular damage. It has become clear that even if
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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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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