Related Experiment Video
Updated: Apr 27, 2026

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Innate and adaptive immune responses subsequent to ischemia-reperfusion injury in the kidney
1Transplant Surgery Research Laboratory and Division of Transplant Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Department of Visceral, Transplantation and Thoracic Surgery, Medical University, Innsbruck, Austria.
Abstract:
Understanding innate immune responses and their correlation to alloimmunity after solid organ transplantation is key to optimizing long term graft outcome. While Ischemia/Reperfusion injury (IRI) has been well studied, new insight into central mechanisms of innate immune activation, i.e. chemokine mediated cell trafficking and the role of Toll-like receptors have evolved recently. The mechanistic implications of Neutrophils, Macrophages/Monocytes, NK-cells, Dendritic cells in renal IRI has been proven by selective depletion of these cell types, thereby offering novel therapeutic interventions. At the same time, the multi-faceted role of different T-cell subsets in IRI has gained interest, highlighting the dichotomous effects of differentiated T-cells and suggesting more selective therapeutic approaches. Targeting innate immune cells and their activation and migration pathways, respectively, has been promising in experimental models holding translational potential. This review will summarize the effects of innate immune activation and potential strategies to interfere with the immunological cascade following renal IRI.
Related Concept Videos
Acute Kidney Injury II: Pathophysiology
Acute Kidney Injury I: Introduction
Acute Kidney Injury III: Clinical Manifestations
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Acute Kidney Injury V: Interprofessional Care
Kidney Transplant II: Surgical Procedure

