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*
Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104; and
Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21287
Two recombinant Listeria monocytogenes (rLm) strains
were produced that secrete the human papilloma virus-16 (HPV-16) E7
protein expressed in HPV-16-associated cervical cancer cells. One,
Lm-E7, expresses and secretes E7 protein, whereas a second, Lm-LLO-E7,
secretes E7 as a fusion protein joined to a nonhemolytic listeriolysin
O (LLO). Lm-LLO-E7, but not Lm-E7, induces the regression of the
E7-expressing tumor, TC-1, established in syngeneic C57BL/6 mice. Both
recombinant E7-expressing rLm vaccines induce measurable anti-E7
CTL responses that stain positively for H-2Db E7 tetramers.
Depletion of the CD8+ T cell subset before treatment
abrogates the ability of Lm-LLO-E7 to impact on tumor growth. In
addition, the rLm strains induce markedly different CD4+ T
cell subsets. Depletion of the CD4+ T cell subset
considerably reduces the ability of Lm-LLO-E7 to eliminate established
TC-1 tumors. Surprisingly, the reverse is the case for Lm-E7, which
becomes an effective anti-tumor immunotherapeutic in mice lacking
this T cell subset. Ab-mediated depletion of TGF-
and
CD25+ cells improves the effectiveness of Lm-E7 treatment,
suggesting that TGF- and CD25+ cells are in part
responsible for this suppressive response. CD4+ T cells
from mice immunized with Lm-E7 are capable of suppressing the ability
of Lm-LLO-E7 to induce the regression of TC-1 when transferred to
tumor-bearing mice. These studies demonstrate the complexity of
L. monocytogenes-mediated tumor immunotherapy targeting
the human tumor Ag, HPV-16 E7.
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