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Immunological consequences of kidney cell death.

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eMediNexus    05 February 2018

A new article published in Cell Death & Disease reported that death of renal cells is the primary etiological factor in the pathophysiology of acute tubular necrosis, autoimmunity, necrotizing glomerulonephritis, cystic kidney disease, urosepsis, delayed graft function, and transplant rejection. The article elaborated that via regulated necrosis, immunogenic damage-associated molecular patterns (DAMPs) and highly reactive organelles such as lysosomes, peroxisomes and mitochondria are released from the dying cells, causing an overwhelming immunologic response. Additionally, the rupture of plasma membrane exhibits irreversibility for the immunogenicity of regulated cell death, hence apoptosis – a highly organized cell death, fails to elicit an immune response. On the other hand, ferroptosis – an iron-dependent necrotic type cell death, results in the release of DAMPs and large amounts of lipid peroxides. Whereas, anti-inflammatory cytokines are actively released from cells that die by necroptosis, limiting the DAMP-induced immune response to a surrounding microenvironment; meanwhile, inflammasome-associated caspases drive maturation of intracellularly expressed interleukin-1β (IL-1β). In summary, this article provided an overview of regulated necrosis in kidney diseases with a focus on immunogenicity and potential therapeutic interventions.

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