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Providence of the CD25+ KIR+ CD127- FOXP3- CD8+ T-cell subset determines the dynamics of tumor immune surveillance.
Immunol Cell Biol 2018; 96(10):1035-1048IC

Abstract

CD8+ T-regulatory (Treg) cells are emerging as crucial components of immune system. Previous studies have reported the presence of FOXP3+ CD8+ Treg cells, similar to CD4+ Tregs, in cancer patients which produce high levels of the immunosuppressive cytokines, IL10 and TGFβ. At an early stage of tumor development, we have identified a subset of FOXP3- CD8+ CD25+ KIR+ CD127- Treg-like cells, which are IFNγ+ . However, this early-induced CD8+ CD25+ CD127- T-cell subset is certainly distinct from the IFNγ+ CD8+ T-effector cells. These CD8+ CD25+ CD127- T cells express other FOXP3- CD8+ Treg cell signature markers, and can selectively suppress autoreactive HLA-E+ TFH cells as well as tumor-induced CD4+ Treg cells. In contrast to FOXP3+ CD8+ Tregs, this subset does not inhibit effector T-cell proliferation or their functions as they are HLA-E- . Adoptive transfer of this early-CD8+ Treg-like subset restrained tumor growth and inhibited CD4+ Treg generation that impedes the immune surveillance and impairs cancer immunotherapy. At the late stage of tumor development, when CD4+ Treg cells dominate the tumor-microenvironment, CD4+ Tregs mediate the clonal deletion of these tumor-suppressive FOXP3- IFNγ+ CD8+ CD25+ CD127- T cells and ensure tumor immune evasion. Our findings suggest that at an early stage of the tumor, this tumor-induced IFNγ-producing FOXP3- CD8+ CD25+ CD127- T-cell subset can potentiate immune surveillance by targeting HLA-E-restricted CD4+ Treg cells while leaving the effector T-cell population unaffected. Hence, manipulating their profile can open up a new avenue in cancer immunotherapy.

Authors+Show Affiliations

Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, 700 054, India.Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, 700 054, India.Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, 700 054, India.Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, 700 054, India.Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, 700 054, India.Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, 700 054, India.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29768737

Citation

Chakraborty, Sreeparna, et al. "Providence of the CD25+ KIR+ CD127- FOXP3- CD8+ T-cell Subset Determines the Dynamics of Tumor Immune Surveillance." Immunology and Cell Biology, vol. 96, no. 10, 2018, pp. 1035-1048.
Chakraborty S, Bhattacharjee P, Panda AK, et al. Providence of the CD25+ KIR+ CD127- FOXP3- CD8+ T-cell subset determines the dynamics of tumor immune surveillance. Immunol Cell Biol. 2018;96(10):1035-1048.
Chakraborty, S., Bhattacharjee, P., Panda, A. K., Kajal, K., Bose, S., & Sa, G. (2018). Providence of the CD25+ KIR+ CD127- FOXP3- CD8+ T-cell subset determines the dynamics of tumor immune surveillance. Immunology and Cell Biology, 96(10), pp. 1035-1048. doi:10.1111/imcb.12166.
Chakraborty S, et al. Providence of the CD25+ KIR+ CD127- FOXP3- CD8+ T-cell Subset Determines the Dynamics of Tumor Immune Surveillance. Immunol Cell Biol. 2018;96(10):1035-1048. PubMed PMID: 29768737.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Providence of the CD25+ KIR+ CD127- FOXP3- CD8+ T-cell subset determines the dynamics of tumor immune surveillance. AU - Chakraborty,Sreeparna, AU - Bhattacharjee,Pushpak, AU - Panda,Abir K, AU - Kajal,Kirti, AU - Bose,Sayantan, AU - Sa,Gaurisankar, Y1 - 2018/08/17/ PY - 2017/08/17/received PY - 2018/05/05/revised PY - 2018/05/07/accepted PY - 2018/5/17/pubmed PY - 2019/7/18/medline PY - 2018/5/17/entrez KW - FOXP3 KW - IFNγ KW - Treg cells KW - immunosurvillance KW - tumor SP - 1035 EP - 1048 JF - Immunology and cell biology JO - Immunol. Cell Biol. VL - 96 IS - 10 N2 - CD8+ T-regulatory (Treg) cells are emerging as crucial components of immune system. Previous studies have reported the presence of FOXP3+ CD8+ Treg cells, similar to CD4+ Tregs, in cancer patients which produce high levels of the immunosuppressive cytokines, IL10 and TGFβ. At an early stage of tumor development, we have identified a subset of FOXP3- CD8+ CD25+ KIR+ CD127- Treg-like cells, which are IFNγ+ . However, this early-induced CD8+ CD25+ CD127- T-cell subset is certainly distinct from the IFNγ+ CD8+ T-effector cells. These CD8+ CD25+ CD127- T cells express other FOXP3- CD8+ Treg cell signature markers, and can selectively suppress autoreactive HLA-E+ TFH cells as well as tumor-induced CD4+ Treg cells. In contrast to FOXP3+ CD8+ Tregs, this subset does not inhibit effector T-cell proliferation or their functions as they are HLA-E- . Adoptive transfer of this early-CD8+ Treg-like subset restrained tumor growth and inhibited CD4+ Treg generation that impedes the immune surveillance and impairs cancer immunotherapy. At the late stage of tumor development, when CD4+ Treg cells dominate the tumor-microenvironment, CD4+ Tregs mediate the clonal deletion of these tumor-suppressive FOXP3- IFNγ+ CD8+ CD25+ CD127- T cells and ensure tumor immune evasion. Our findings suggest that at an early stage of the tumor, this tumor-induced IFNγ-producing FOXP3- CD8+ CD25+ CD127- T-cell subset can potentiate immune surveillance by targeting HLA-E-restricted CD4+ Treg cells while leaving the effector T-cell population unaffected. Hence, manipulating their profile can open up a new avenue in cancer immunotherapy. SN - 1440-1711 UR - https://www.unboundmedicine.com/medline/citation/29768737/Providence_of_the_CD25+_KIR+_CD127__FOXP3__CD8+_T_cell_subset_determines_the_dynamics_of_tumor_immune_surveillance_ L2 - https://doi.org/10.1111/imcb.12166 DB - PRIME DP - Unbound Medicine ER -