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Updated: Aug 7, 2026
Isolation and Expansion of Cytotoxic Cytokine-induced Killer T Cells for Cancer Treatment
Published on: January 24, 2020
Antitumor effect by interleukin-11 receptor alpha-locus chemokine/CCL27, introduced into tumor cells through a
Jian-Qing Gao1, Yasuhiro Tsuda, Kazufumi Katayama
1Department of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka 565-0871, Japan.
Abstract:
In this study, we examined antitumor activity of a mouse CC chemokine ILC/CCL27 and a mouse CX(3)C chemokine fractalkine/CX(3)CL1 in vivo. We generated recombinant adenovirus vectors with a fiber mutation, encoding mILC (Ad-RGD-mILC) and mFKN (Ad-RGD-mFKN). We confirmed tumor cells infected with Ad-RGD-mILC and Ad-RGD-mFKN to express and release these chemokines. Tumor rejection experiments in vivo were carried out by inoculating OV-HM cells infected with Ad-RGD-mILC or Ad-RGD-mFKN into immunocompetent mice. mILC significantly suppressed the tumor growth, whereas no such significant effect was observed by mFKN. The antitumor activity induced by mILC was T cell dependent, involving both CD4(+) and CD8(+) T cells. Immunohistochemical analysis revealed accumulation of both CD3(+) lymphocytes and NK cells in the tumor tissue transduced with mILC and mFKN. However, there was a significant difference in the distribution of infiltrating cells. Furthermore, mFKN appeared to have an angiogenic activity, which might have masked its tumor suppressive activity. Collectively, ILC/CCL27 may be a good candidate molecule for cancer gene therapy.
Insights
Mouse CC chemokine ILC/CCL27 demonstrated significant antitumor activity in vivo, mediated by T cells. Mouse CX(3)C chemokine fractalkine/CX(3)CL1 showed no significant effect, suggesting ILC/CCL27 is a promising candidate for cancer gene therapy.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- Chemokines play crucial roles in immune responses and cancer.
- Investigating the in vivo antitumor potential of specific chemokines is essential for developing novel cancer therapies.
Purpose of the Study:
- To evaluate the in vivo antitumor activity of mouse CC chemokine ILC/CCL27 and mouse CX(3)C chemokine fractalkine/CX(3)CL1.
- To determine the immune mechanisms underlying the antitumor effects.
Main Methods:
- Generation of recombinant adenovirus vectors encoding mouse ILC/CCL27 (Ad-RGD-mILC) and mouse fractalkine/CX(3)CL1 (Ad-RGD-mFKN).
- Inoculation of chemokine-expressing tumor cells into immunocompetent mice for in vivo tumor rejection experiments.
- Immunohistochemical analysis to assess immune cell infiltration and distribution.
Main Results:
- Ad-RGD-mILC significantly suppressed tumor growth, while Ad-RGD-mFKN did not show a significant effect.
- The antitumor activity of mILC/CCL27 was dependent on CD4(+) and CD8(+) T cells.
- Both chemokines induced infiltration of CD3(+) lymphocytes and NK cells, but with different distribution patterns.
- Fractalkine/CX(3)CL1 exhibited angiogenic activity, potentially masking its tumor suppressive effects.
Conclusions:
- Mouse ILC/CCL27 exhibits potent, T cell-dependent antitumor activity.
- Fractalkine/CX(3)CL1's potential antitumor effects may be counteracted by its angiogenic properties.
- ILC/CCL27 is a promising candidate molecule for cancer gene therapy.
