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Induction of systemic immunity by expression of interleukin‐23 in murine colon carcinoma cells
Author(s) -
Wang YanQing,
Ugai Shinichi,
Shimozato Osamu,
Yu Ling,
Kawamura Kiyoko,
Yamamoto Hiroshi,
Yamaguchi Taketo,
Saisho Hiromitsu,
Tagawa Masatoshi
Publication year - 2003
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.11160
Subject(s) - cytokine , spleen , cd8 , colon carcinoma , interleukin 12 , immunity , cellular immunity , biology , cancer research , in vitro , immunology , colorectal cancer , medicine , immune system , cytotoxic t cell , cancer , biochemistry
Interleukin‐23 (IL‐23), a novel cytokine composed of a newly identified p19 molecule and the p40 subunit of IL‐12, can stimulate the proliferation in vitro of memory T cells. We examined whether Colon 26 murine colon carcinoma cells that were retrovirally transduced with the p19 ‐linked p40 gene (Colon 26/IL‐23) could produce antitumor effects in inoculated mice. The growth of Colon 26/IL‐23 tumors developed in immunocompetent mice was significantly retarded and the tumors disappeared thereafter. Spleen cells from the mice that received Colon 26/IL‐23 cells produced significant amounts of interferon‐γ, when they were cultured with irradiated Colon 26 but not irrelevant cells. Depletion of CD8 + T cells suppressed the production of interferon‐γ. The mice that had rejected Colon 26/IL‐23 tumors were resistant to subsequent challenge of parent but not irrelevant tumor cells. Colon 26/IL‐23 tumors were not rejected in nude mice but the growth was retarded compared to parent tumors. Treatment of nude mice with anti‐asialo GM 1 antibody did not influence the growth of Colon 26/IL‐23 tumors. These data suggest that expression of IL‐23 in tumors produces T cell‐dependent antitumor effects and induces systemic immunity. © 2003 Wiley‐Liss, Inc.