抄録
Although tumor antigen-specific immunotherapy, such as dendritic cell vaccine, has recently emerged as a promising clinical approach, one limitation of tumor antigen- and T-cell receptor (TcR)- specific immunotherapy is antigen-specific inhibition by antigen-specific regulatory T-cell and myeloid suppressor cells. Therefore, immunotherapy using a TcR-independent mechanism may be an alternative immunotherapeutic strategy. NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells. Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting. Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia. Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 2241-2247 |
| ページ数 | 7 |
| ジャーナル | Anticancer Research |
| 巻 | 32 |
| 発行部数 | 6 |
| 出版物ステータス | 出版済み - 6 2012 |
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All Science Journal Classification (ASJC) codes
- Cancer Research
- Oncology
これを引用
Cancer immunotherapy using NKG2D and DNAM-1 systems. / Morisaki, Takashi; Ohnishi, Hideya; Katano, Mitsuo.
：: Anticancer Research, 巻 32, 番号 6, 06.2012, p. 2241-2247.研究成果: ジャーナルへの寄稿 › 評論記事
}
TY - JOUR
T1 - Cancer immunotherapy using NKG2D and DNAM-1 systems
AU - Morisaki, Takashi
AU - Ohnishi, Hideya
AU - Katano, Mitsuo
PY - 2012/6
Y1 - 2012/6
N2 - Although tumor antigen-specific immunotherapy, such as dendritic cell vaccine, has recently emerged as a promising clinical approach, one limitation of tumor antigen- and T-cell receptor (TcR)- specific immunotherapy is antigen-specific inhibition by antigen-specific regulatory T-cell and myeloid suppressor cells. Therefore, immunotherapy using a TcR-independent mechanism may be an alternative immunotherapeutic strategy. NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells. Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting. Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia. Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
AB - Although tumor antigen-specific immunotherapy, such as dendritic cell vaccine, has recently emerged as a promising clinical approach, one limitation of tumor antigen- and T-cell receptor (TcR)- specific immunotherapy is antigen-specific inhibition by antigen-specific regulatory T-cell and myeloid suppressor cells. Therefore, immunotherapy using a TcR-independent mechanism may be an alternative immunotherapeutic strategy. NKG2D (natural killer, group 2, member D) and DNAX accessory molecule-1 (DNAM-1) are both activated receptors that are strongly expressed on T-cells, γδT-cells, and NK cells. Therefore, the expression of ligands for NKG2D and DNAM-1 on tumor cells plays an important role in tumor opsonization by immune effector cell targeting. Various modulatory methods for up-regulating NKG2D and DNAM-1-ligands have been reported, and included chemotherapeutic agents and hyperthermia. Although there are many obstacles to the utilization of NKG2D and DNAM-1 for cancer therapy, combined treatments using immune cell therapy and chemotherapy that take advantage of NKG2D and DNAM-1 may be an ideal approach.
UR - http://www.scopus.com/inward/record.url?scp=84864530880&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84864530880&partnerID=8YFLogxK
M3 - Review article
C2 - 22641658
AN - SCOPUS:84864530880
VL - 32
SP - 2241
EP - 2247
JO - Anticancer Research
JF - Anticancer Research
SN - 0250-7005
IS - 6
ER -