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Granzyme‐b mediated cell death in the spinal cord‐injured rat model
Author(s) -
Chaitanya Ganta Vijay,
Kolli Mayuri,
Babu Phanithi Prakash
Publication year - 2009
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/j.1440-1789.2008.00980.x
Subject(s) - granzyme b , spinal cord , cytotoxic t cell , spinal cord injury , cxcl10 , programmed cell death , chemokine , medicine , granzyme , immune system , biology , apoptosis , immunology , t cell , perforin , cd8 , neuroscience , in vitro , biochemistry
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.