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Prepublished online as a Blood First Edition Paper on December 19, 2002; DOI 10.1182/blood-2002-08-2485.
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Blood, 15 April 2003, Vol. 101, No. 8, pp. 3093-3101
IMMUNOBIOLOGY
Cell death induced by granzyme C
Hillary Johnson,
Luca Scorrano,
Stanley J. Korsmeyer, and
Timothy J. Ley
From the Division of Oncology, Departments of Medicine
and Genetics, Siteman Cancer Center, Washington University School of
Medicine, St Louis, MO; Howard Hughes Medical Institute, Department of
Pathology and Medicine, Harvard Medical School, Dana Farber Cancer
Institute, Boston, MA.
Although the functions of granzymes A and B have been defined, the
functions of the other highly expressed granzymes (Gzms) of murine
cytotoxic lymphocytes (C, D, and F) have not yet been evaluated. In
this report, we describe the ability of murine GzmC (which is most
closely related to human granzyme H) to cause cell death. The induction
of death requires its protease activity and is characterized by the
rapid externalization of phosphatidylserine, nuclear condensation and
collapse, and single-stranded DNA nicking. The kinetics of these events
are similar to those caused by granzyme B, and its potency (defined on
a molar basis) is also equivalent. The induction of death did not
involve the activation of caspases, the cleavage of BID, or the
activation of the CAD nuclease. However, granzyme C did cause rapid
mitochondrial swelling and depolarization in intact cells or in
isolated mitochondria, and this mitochondrial damage was not prevented
by cyclosporin A pretreatment. These results suggest that granzyme C
rapidly induces target cell death by attacking nuclear and
mitochondrial targets and that these targets are distinct from those
used by granzyme B to cause classical apoptosis.
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