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lüll Ischemia-reperfusion and immediate T cell responses Huang Y; Rabb H; Womer KLCell Immunol 2007[Jul]; 248 (1): 4-11The 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.|Animals[MESH]|Brain Ischemia/physiopathology[MESH]|CD4-Positive T-Lymphocytes/*immunology[MESH]|CD8-Positive T-Lymphocytes/*immunology[MESH]|Cell Adhesion/immunology[MESH]|Complement Pathway, Alternative[MESH]|Complement System Proteins[MESH]|Cytokines/biosynthesis/immunology[MESH]|Dendritic Cells/immunology[MESH]|Disease Models, Animal[MESH]|Humans[MESH]|Hypoxia/immunology[MESH]|Immunity, Innate[MESH]|Kidney/blood supply[MESH]|Liver/blood supply[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Myocardial Ischemia/immunology[MESH]|Neutrophils/cytology/immunology[MESH]|Reperfusion Injury/*immunology[MESH]|T-Lymphocyte Subsets/*immunology[MESH]|T-Lymphocytes, Cytotoxic/immunology[MESH] |