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Death9stitch

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As an even more important protective effect.171,172 Together, these results therefore indicate a potential role for both IL-1 and IL-1 in atherosclerosis. Perhaps, the greater effect of IL-1 in the development of aortic plaques might be in part attributed to the fact that IL-1 deficiency induces the decreased expression of IL-1,172 thereby not only acting on IL-1-dependent cell signaling but also
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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
1
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
1
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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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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As an even more important protective effect.171,172 Together, these results therefore indicate a potential role for both IL-1 and IL-1 in atherosclerosis. Perhaps, the greater effect of IL-1 in the development of aortic plaques might be in part attributed to the fact that IL-1 deficiency induces the decreased expression of IL-1,172 thereby not only acting on IL-1-dependent cell signaling but also
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Ple sclerosis.158?60 Thus, platelet-originating IL-1 would be an early signal playing a central role in the establishment of cerebrovascular inflammation and subsequently devastating brain injury. Notably, similar mechanisms are involved in the ischemic heart following myocardial infarction. Indeed, IL-1 release from necrotic myocytes was shown to trigger acute inflammation by activating surroundi