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Blood, 15 March 2002, Vol. 99, No. 6, pp. 2114-2121
IMMUNOBIOLOGY
Interleukin-17 inhibits tumor cell growth by means of a
T-cell-dependent mechanism
Fabrice Benchetrit,
Arnaud Ciree,
Virginie Vives,
Guy Warnier,
Alain Gey,
Catherine Sautès-Fridman,
François Fossiez,
Nacilla Haicheur,
Wolf H. Fridman, and
Eric Tartour
From INSERM U 255, Université Pierre et Marie
Curie, Hopital Européen Georges Pompidou, Paris, France; Institut
Ludwig for Cancer Research, Brussels Branch, Belgium; and Schering
Plough, Dardilly, France.
Interleukin 17 (IL-17) is a proinflammatory cytokine produced by
activated CD4+ memory T cells. We previously showed that
IL-17 increased the growth rate of human cervical tumors transplanted
into athymic nude mice. To address the possible role of T cells in the
biologic activity of IL-17 for tumor control, we grafted 2 murine
hematopoietic immunogenic tumors (P815 and J558L) transfected with a
complementary DNA encoding murine IL-17 into syngeneic immunocompetent
mice. We found that growth of the 2 IL-17-producing tumors was
significantly inhibited compared with that of mock-transfected tumors.
In contrast to the antitumor activity of IL-17 observed in
immunocompetent mice, we observed no difference in the in vivo growth
of IL-17-transfected or mock-transfected P815 cells (P815-IL-17 and
P815-Neo, respectively) transplanted into nude mice. We then showed
that IL-17 increased generation of specific cytolytic T lymphocytes
(CTLs) directed against the immunodominant antigens from P815 called A,
B, C, D, and E, since all mice injected with P815-IL-17 developed a P815-specific CTL response, whereas only 6 of 16 mice immunized with
P815-Neo had a specific CTL response against the antigens. The
induction of CTLs was associated with establishment of a
tumor-protective immunity. These experiments suggest that T lymphocytes
are involved in the antitumor activity of IL-17. Therefore, IL-17, like
other cytokines, appears to be a pleiotropic cytokine with possible protumor or antitumor effects on tumor development, which often depends
on the immunogenicity of tumor models.
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