Regulatory T cells in cancer immunotherapy
FOXP3-expressing regulatory T （Treg） cells, which suppress aberrant immune response against self-antigens, also suppress anti-tumor immune response. Infiltration of a large number of Treg cells into tumor tissues is often associ- ated with poor prognosis. There is accumulating evidence that the remo...
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| Published in | Cell research Vol. 27; no. 1; pp. 109 - 118 |
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| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.01.2017
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Summary: | FOXP3-expressing regulatory T （Treg） cells, which suppress aberrant immune response against self-antigens, also suppress anti-tumor immune response. Infiltration of a large number of Treg cells into tumor tissues is often associ- ated with poor prognosis. There is accumulating evidence that the removal of Treg cells is able to evoke and enhance anti-tumor immune response. However, systemic depletion of Treg cells may concurrently elicit deleterious autoim- munity. One strategy for evoking effective tumor immunity without antoimmunity is to specifically target terminally differentiated effector Treg cells rather than all FOXP3＋ T cells, because effector Treg cells are the predominant cell type in tumor tissues. Various cell surface molecules, including chemokine receptors such as CCR4, that are specifi- cally expressed by effector Treg cells can be the candidates for depleting effector Treg cells by specific cell-depleting monoclonal antibodies. In addition, other immunological characteristics of effector Treg cells, such as their high ex- pression of CTLA-4, active proliferation, and apoptosis-prone tendency, can be exploited to control specifically their functions. For example, anti-CTLA-4 antibody may kill effector Treg ceils or attenuate their suppressive activity. It is hoped that combination of Treg-cell targeting （e.g., by reducing Treg cells or attenuating their suppressive activity in tumor tissues） with the activation of tumor-specific effector T cells （e.g., by cancer vaccine or immune checkpoint blockade） will make the current cancer immunotherapy more effective. |
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| Bibliography: | FOXP3-expressing regulatory T （Treg） cells, which suppress aberrant immune response against self-antigens, also suppress anti-tumor immune response. Infiltration of a large number of Treg cells into tumor tissues is often associ- ated with poor prognosis. There is accumulating evidence that the removal of Treg cells is able to evoke and enhance anti-tumor immune response. However, systemic depletion of Treg cells may concurrently elicit deleterious autoim- munity. One strategy for evoking effective tumor immunity without antoimmunity is to specifically target terminally differentiated effector Treg cells rather than all FOXP3＋ T cells, because effector Treg cells are the predominant cell type in tumor tissues. Various cell surface molecules, including chemokine receptors such as CCR4, that are specifi- cally expressed by effector Treg cells can be the candidates for depleting effector Treg cells by specific cell-depleting monoclonal antibodies. In addition, other immunological characteristics of effector Treg cells, such as their high ex- pression of CTLA-4, active proliferation, and apoptosis-prone tendency, can be exploited to control specifically their functions. For example, anti-CTLA-4 antibody may kill effector Treg ceils or attenuate their suppressive activity. It is hoped that combination of Treg-cell targeting （e.g., by reducing Treg cells or attenuating their suppressive activity in tumor tissues） with the activation of tumor-specific effector T cells （e.g., by cancer vaccine or immune checkpoint blockade） will make the current cancer immunotherapy more effective. 31-1568 Treg; CTLA-4; cancer; immunotherapy ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
| ISSN: | 1001-0602 1748-7838 1748-7838 |
| DOI: | 10.1038/cr.2016.151 |