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Blood, 1 June 2001, Vol. 97, No. 11, pp. 3505-3512
IMMUNOBIOLOGY
Stressed apoptotic tumor cells express heat shock proteins and
elicit tumor-specific immunity
Hanping Feng,
Yi Zeng,
Luke Whitesell, and
Emmanuel Katsanis
From the Department of Pediatrics, Steele Memorial
Children's Research Center, University of Arizona, Tucson.
In attempting to develop effective anticancer immunotherapies, the
relative ability of apoptotic cells to induce an immune response
remains an important but controversial consideration. A novel
gene-transfer approach was used by which rapid induction of pure
apoptosis can be selectively achieved in a transfected tumor cell
population following exposure to a semisynthetic dimerizing ligand,
AP20187. Inoculation of BALB/c mice with apoptotic and viable 12B1-D1
leukemia cells, at a 12:1 ratio subcutaneously, led to early tumor
growth. Heat stress up-regulated the expression of membrane heat shock
proteins (HSP72 and HSP60) on apoptotic 12B1-D1 cells, and
stressed apoptotic cells were capable of generating a T-cell-mediated
specific antitumor response. Pulsing of stressed apoptotic leukemia
cells onto syngeneic dendritic cells resulted largely in rejection of
coinjected viable 12B1-D1 cells. Mice rejecting the primary 12B1-D1
inoculum were immune to the same but not to a different leukemia
challenge. Our findings indicate that tumor immunogenicity is dependent
on whether cells are stressed before apoptosis induction and suggest
that the immune system is capable of distinguishing between stressed
and nonstressed cells undergoing programmed cell death.
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