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N, joints and bones. Systemic treatment with recombinant IL-1Ra (anakinra) has been an efficient way to decrease inflammation and prevent death.156 However, because anakinra can inhibit both IL-1 and IL-1 by binding to their common receptor, it is unclear which is the main cytokine at the root of the sterile inflammation affecting these patients. Nonetheless, anakinra is currently also used to tre
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N, joints and bones. Systemic treatment with recombinant IL-1Ra (anakinra) has been an efficient way to decrease inflammation and prevent death.156 However, because anakinra can inhibit both IL-1 and IL-1 by binding to their common receptor, it is unclear which is the main cytokine at the root of the sterile inflammation affecting these patients. Nonetheless, anakinra is currently also used to tre
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E, this time with a clear aim at blocking IL-1-derived inflammation.156 Yet, some evidence suggests a role for IL-1 in the development of these chronic inflammatory diseases. In fact, early IL-1 release is recognized as an important step that initiates inflammation, and IL-1 is thus considered a promising target for the treatment of rheumatologic disease.156,164 Interestingly, RA patients producin
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E, this time with a clear aim at blocking IL-1-derived inflammation.156 Yet, some evidence suggests a role for IL-1 in the development of these chronic inflammatory diseases. In fact, early IL-1 release is recognized as an important step that initiates inflammation, and IL-1 is thus considered a promising target for the treatment of rheumatologic disease.156,164 Interestingly, RA patients producin
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Otentiating its proinflammatory activity.144 Interestingly, IL-1 may also be displayed at the cell surface, where it can activate juxtaposing target cells expressing its receptor, such as T cells or endothelial cells (Figure 2).145?48 As for IL-1, once it is released into the extracellular space, soluble or membrane-bound IL-1 binds to IL-1R1 and further triggers the recruitment of the accessory r
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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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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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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