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      Granzyme-b mediated cell death in the spinal cord-injured rat model.

      Neuropathology : official journal of the Japanese Society of Neuropathology
      Animals, Antigens, CD8, metabolism, Cell Death, Cerebellum, Chemokine CXCL10, Granzymes, Male, Neurons, physiology, Phosphopyruvate Hydratase, Poly(ADP-ribose) Polymerases, Rats, Rats, Wistar, Spinal Cord Injuries, physiopathology, T-Lymphocytes, Time Factors

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          Abstract

          Spinal cord injury initiates a complex series of inflammatory and immune responses including the influx of monocytes, macrophages, T-cells, NK cells and so on, into the injured area. In the present study, we found a significant increase in the levels of granzyme-b (gra-b) from the first day after the transection until the third day, with decrease in intensity thereafter. The chemokine IP-10/CXCL10 was also found to be elevated along with gra-b correlating with the infiltration of CD-8(+) cytotoxic T lymphocytes (CTLs) into the injured spinal cord. We observed an increase in the levels of the 64 kDa poly ADP ribose polymerase fragment, known to be a signature fragment produced by gra-b. Localization of gra-b in TUNEL positive neurons indicates that gra-b might play a crucial role in neuronal death and contributes to the pathophysiology of spinal cord injury.

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