Ischemia-reperfusion (IR) injury involving harvested organs and allograft transplantation may be increased by stimulation of a newly described innate pro-inflammatory immune system (i.e.NALP-3-inflammasome) which can cause secretion of IL-1.beta. and subsequent neutrophilic inflammation. Ischemia and hypoxia can cause metabolic acidosis and development of danger signals known to stimulate IL-1.beta. secretion from the NALP-3 inflammasome. Based on this newly discovered mechanism causing pathobiology in IRI, IL-1.beta. targeted therapy would be capable of improving allograft tolerance, viability of harvested organs and in conditions with compromised arterial blood supply and subsequent reperfusion, such as replants, compartment syndrome, and serious vascular accidents.

Wanderer; Alan Anson

Rationale for IL-1 .beta. targeted therapy to improve harvested organ viability, allograft tolerance, replant success and for conditions characterized by reduced or absent arterial perfusion

compartment syndromes/hypoxia

Rationale for IL-1 .beta. targeted therapy to improve harvested organ viability, allograft tolerance, replant success and for conditions characterized by reduced or absent arterial perfusion

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