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Updated: Jul 10, 2026

Delayed Intramyocardial Delivery of Stem Cells after Ischemia Reperfusion Injury in a Murine Model
Published on: September 3, 2020
Ischemia-reperfusion and immediate T cell responses
Yanfei Huang1, Hamid Rabb, Karl L Womer
1Division of Nephrology, Johns Hopkins University School of Medicine, Ross 965, 720 Rutland Avenue, Baltimore, MD 21205, USA.
The pathogenesis of ischemia-reperfusion injury (IRI) is complex and not well understood. Inflammation plays an important role in IRI, with involvement of leukocytes, adhesion molecules, chemokines and cytokines. Emerging data suggest a role of T cells as mediators of IRI both in renal and extra-renal organs. Divergent roles of T cell subsets have also been elucidated, suggesting a more complicated role of T cells in the different phases of IRI. This review presents recent evidence from various animal models that advances our understanding of the role T cells play in IRI. These findings entertain the possibility of using immunotherapeutic agents for the prevention and treatment of IRI.
The pathogenesis of ischemia-reperfusion injury (IRI) is complex and not well understood. Inflammation plays an important role in IRI, with involvement of leukocytes, adhesion molecules, chemokines and cytokines. Emerging data suggest a role of T cells as mediators of IRI both in renal and extra-renal organs. Divergent roles of T cell subsets have also been elucidated, suggesting a more complicated role of T cells in the different phases of IRI. This review presents recent evidence from various animal models that advances our understanding of the role T cells play in IRI. These findings entertain the possibility of using immunotherapeutic agents for the prevention and treatment of IRI.
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