Vδ2 T cell subsets, defined by PD-1 and TIM-3 expression, present varied cytokine responses in acute myeloid leukemia patients
•The levels of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients.•PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ expression.•PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression.•Anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition elevated TNF-α and IFN-...
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| Published in | International immunopharmacology Vol. 80; p. 106122 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.03.2020
Elsevier BV |
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| Abstract | •The levels of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients.•PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ expression.•PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression.•Anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition elevated TNF-α and IFN-γ.•Anti-PD-1 blocking antibodies increased the frequency of TIM-3+ cells in Vδ2 T cells.
Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In acute myeloid leukemia (AML) patients receiving allogeneic stem cell transplantation, higher γδ T cell count predicted better prognosis. The impact of PD-1 and TIM-3 expression on the function of Vδ2 T cells is yet unclear. In this study, we showed that the frequencies of PD-1+TIM-3− Vδ2 T cells were comparable between healthy controls and AML patients, but the frequencies of PD-1−TIM-3+ Vδ2 T cells and of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients than in healthy controls. Both PD-1 and TIM-3 were upregulated upon phosphoantigen + IL-2 activation, but the relative differences in the frequencies of various PD-1 vs. TIM-3 subsets between AML patients and healthy controls remained. Interestingly, among all PD-1 vs. TIM-3 subsets, the PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ expression, while the PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression. Anti-PD-1 inhibition did not significantly affect the production of TNF-α or IFN-γ, but anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition significantly elevated the production of TNF-α and IFN-γ. Interestingly, anti-PD-1 blocking antibodies had significantly increased the frequency of TIM-3+ cells in Vδ2 T cells, suggesting a compensatory TIM-3 upregulation. In addition, the levels of PD-L1 and HMGB-1 were significantly higher in AML patients than in healthy subjects. In summary, this study provides knowledge on the cytokine expression patterns by PD-1 and/or TIM-3-expressing Vδ2 T cells in AML patients, and indicates that the upregulation of PD-1 alone is insufficient to indicate functional impairment, and Vδ2 T cells may require anti-TIM-3 inhibition for functional revival. |
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| AbstractList | •The levels of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients.•PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ expression.•PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression.•Anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition elevated TNF-α and IFN-γ.•Anti-PD-1 blocking antibodies increased the frequency of TIM-3+ cells in Vδ2 T cells.
Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In acute myeloid leukemia (AML) patients receiving allogeneic stem cell transplantation, higher γδ T cell count predicted better prognosis. The impact of PD-1 and TIM-3 expression on the function of Vδ2 T cells is yet unclear. In this study, we showed that the frequencies of PD-1+TIM-3− Vδ2 T cells were comparable between healthy controls and AML patients, but the frequencies of PD-1−TIM-3+ Vδ2 T cells and of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients than in healthy controls. Both PD-1 and TIM-3 were upregulated upon phosphoantigen + IL-2 activation, but the relative differences in the frequencies of various PD-1 vs. TIM-3 subsets between AML patients and healthy controls remained. Interestingly, among all PD-1 vs. TIM-3 subsets, the PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ expression, while the PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression. Anti-PD-1 inhibition did not significantly affect the production of TNF-α or IFN-γ, but anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition significantly elevated the production of TNF-α and IFN-γ. Interestingly, anti-PD-1 blocking antibodies had significantly increased the frequency of TIM-3+ cells in Vδ2 T cells, suggesting a compensatory TIM-3 upregulation. In addition, the levels of PD-L1 and HMGB-1 were significantly higher in AML patients than in healthy subjects. In summary, this study provides knowledge on the cytokine expression patterns by PD-1 and/or TIM-3-expressing Vδ2 T cells in AML patients, and indicates that the upregulation of PD-1 alone is insufficient to indicate functional impairment, and Vδ2 T cells may require anti-TIM-3 inhibition for functional revival. Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In acute myeloid leukemia (AML) patients receiving allogeneic stem cell transplantation, higher γδ T cell count predicted better prognosis. The impact of PD-1 and TIM-3 expression on the function of Vδ2 T cells is yet unclear. In this study, we showed that the frequencies of PD-1 TIM-3 Vδ2 T cells were comparable between healthy controls and AML patients, but the frequencies of PD-1 TIM-3 Vδ2 T cells and of PD-1 TIM-3 Vδ2 T cells were significantly higher in AML patients than in healthy controls. Both PD-1 and TIM-3 were upregulated upon phosphoantigen + IL-2 activation, but the relative differences in the frequencies of various PD-1 vs. TIM-3 subsets between AML patients and healthy controls remained. Interestingly, among all PD-1 vs. TIM-3 subsets, the PD-1 TIM-3 subset presented the highest TNF-α and IFN-γ expression, while the PD-1 TIM-3 subset presented the lowest TNF-α and IFN-γ expression. Anti-PD-1 inhibition did not significantly affect the production of TNF-α or IFN-γ, but anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition significantly elevated the production of TNF-α and IFN-γ. Interestingly, anti-PD-1 blocking antibodies had significantly increased the frequency of TIM-3 cells in Vδ2 T cells, suggesting a compensatory TIM-3 upregulation. In addition, the levels of PD-L1 and HMGB-1 were significantly higher in AML patients than in healthy subjects. In summary, this study provides knowledge on the cytokine expression patterns by PD-1 and/or TIM-3-expressing Vδ2 T cells in AML patients, and indicates that the upregulation of PD-1 alone is insufficient to indicate functional impairment, and Vδ2 T cells may require anti-TIM-3 inhibition for functional revival. Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In acute myeloid leukemia (AML) patients receiving allogeneic stem cell transplantation, higher γδ T cell count predicted better prognosis. The impact of PD-1 and TIM-3 expression on the function of Vδ2 T cells is yet unclear. In this study, we showed that the frequencies of PD-1+TIM-3− Vδ2 T cells were comparable between healthy controls and AML patients, but the frequencies of PD-1−TIM-3+ Vδ2 T cells and of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients than in healthy controls. Both PD-1 and TIM-3 were upregulated upon phosphoantigen + IL-2 activation, but the relative differences in the frequencies of various PD-1 vs. TIM-3 subsets between AML patients and healthy controls remained. Interestingly, among all PD-1 vs. TIM-3 subsets, the PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ expression, while the PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression. Anti-PD-1 inhibition did not significantly affect the production of TNF-α or IFN-γ, but anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition significantly elevated the production of TNF-α and IFN-γ. Interestingly, anti-PD-1 blocking antibodies had significantly increased the frequency of TIM-3+ cells in Vδ2 T cells, suggesting a compensatory TIM-3 upregulation. In addition, the levels of PD-L1 and HMGB-1 were significantly higher in AML patients than in healthy subjects. In summary, this study provides knowledge on the cytokine expression patterns by PD-1 and/or TIM-3-expressing Vδ2 T cells in AML patients, and indicates that the upregulation of PD-1 alone is insufficient to indicate functional impairment, and Vδ2 T cells may require anti-TIM-3 inhibition for functional revival. Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In acute myeloid leukemia (AML) patients receiving allogeneic stem cell transplantation, higher γδ T cell count predicted better prognosis. The impact of PD-1 and TIM-3 expression on the function of Vδ2 T cells is yet unclear. In this study, we showed that the frequencies of PD-1+TIM-3- Vδ2 T cells were comparable between healthy controls and AML patients, but the frequencies of PD-1-TIM-3+ Vδ2 T cells and of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients than in healthy controls. Both PD-1 and TIM-3 were upregulated upon phosphoantigen + IL-2 activation, but the relative differences in the frequencies of various PD-1 vs. TIM-3 subsets between AML patients and healthy controls remained. Interestingly, among all PD-1 vs. TIM-3 subsets, the PD-1+TIM-3- subset presented the highest TNF-α and IFN-γ expression, while the PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression. Anti-PD-1 inhibition did not significantly affect the production of TNF-α or IFN-γ, but anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition significantly elevated the production of TNF-α and IFN-γ. Interestingly, anti-PD-1 blocking antibodies had significantly increased the frequency of TIM-3+ cells in Vδ2 T cells, suggesting a compensatory TIM-3 upregulation. In addition, the levels of PD-L1 and HMGB-1 were significantly higher in AML patients than in healthy subjects. In summary, this study provides knowledge on the cytokine expression patterns by PD-1 and/or TIM-3-expressing Vδ2 T cells in AML patients, and indicates that the upregulation of PD-1 alone is insufficient to indicate functional impairment, and Vδ2 T cells may require anti-TIM-3 inhibition for functional revival.Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In acute myeloid leukemia (AML) patients receiving allogeneic stem cell transplantation, higher γδ T cell count predicted better prognosis. The impact of PD-1 and TIM-3 expression on the function of Vδ2 T cells is yet unclear. In this study, we showed that the frequencies of PD-1+TIM-3- Vδ2 T cells were comparable between healthy controls and AML patients, but the frequencies of PD-1-TIM-3+ Vδ2 T cells and of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients than in healthy controls. Both PD-1 and TIM-3 were upregulated upon phosphoantigen + IL-2 activation, but the relative differences in the frequencies of various PD-1 vs. TIM-3 subsets between AML patients and healthy controls remained. Interestingly, among all PD-1 vs. TIM-3 subsets, the PD-1+TIM-3- subset presented the highest TNF-α and IFN-γ expression, while the PD-1+TIM-3+ subset presented the lowest TNF-α and IFN-γ expression. Anti-PD-1 inhibition did not significantly affect the production of TNF-α or IFN-γ, but anti-TIM-3 inhibition and anti-PD-1/TIM-3 dual inhibition significantly elevated the production of TNF-α and IFN-γ. Interestingly, anti-PD-1 blocking antibodies had significantly increased the frequency of TIM-3+ cells in Vδ2 T cells, suggesting a compensatory TIM-3 upregulation. In addition, the levels of PD-L1 and HMGB-1 were significantly higher in AML patients than in healthy subjects. In summary, this study provides knowledge on the cytokine expression patterns by PD-1 and/or TIM-3-expressing Vδ2 T cells in AML patients, and indicates that the upregulation of PD-1 alone is insufficient to indicate functional impairment, and Vδ2 T cells may require anti-TIM-3 inhibition for functional revival. |
| ArticleNumber | 106122 |
| Author | Wu, Kangni Zeng, Hanyan Xiu, Yanghui Xia, Weilin Feng, Juan Yu, Lian Xu, Bing Lin, Zhijuan Zhao, Haijun Li, Zhifeng |
| Author_xml | – sequence: 1 givenname: Kangni surname: Wu fullname: Wu, Kangni organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China – sequence: 2 givenname: Juan surname: Feng fullname: Feng, Juan organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China – sequence: 3 givenname: Yanghui surname: Xiu fullname: Xiu, Yanghui organization: Eye Institute and Xiamen Eye Center Affiliated to Xiamen University, Xiamen, Fujian, China – sequence: 4 givenname: Zhifeng surname: Li fullname: Li, Zhifeng organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China – sequence: 5 givenname: Zhijuan surname: Lin fullname: Lin, Zhijuan organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China – sequence: 6 givenname: Haijun surname: Zhao fullname: Zhao, Haijun organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China – sequence: 7 givenname: Hanyan surname: Zeng fullname: Zeng, Hanyan organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China – sequence: 8 givenname: Weilin surname: Xia fullname: Xia, Weilin organization: Department of Hematology, Jieyang People’s Hospital (JieYang Affiliated Hospital, Sun Yat-sen University), Jieyang, Guangdong, China – sequence: 9 givenname: Lian surname: Yu fullname: Yu, Lian email: yulian_ly@126.com organization: Department of Hematology and Rheumatology, Longyan First Hospital Affiliated to Fujian Medical University, Longyan, Fujian, China – sequence: 10 givenname: Bing surname: Xu fullname: Xu, Bing email: bingxudr@sina.com organization: Department of Hematology, The First Affiliated Hospital of Xiamen University and Institute of Hematology, Medical College of Xiamen University, Xiamen, Fujian, China |
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| Keywords | Vδ2 T cell TIM-3 PD-1 Acute myeloid leukemia |
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| Snippet | •The levels of PD-1+TIM-3+ Vδ2 T cells were significantly higher in AML patients.•PD-1+TIM-3− subset presented the highest TNF-α and IFN-γ... Vδ2 T cells represent the major γδ T cell subset in humans and can serve as an important early source of TNF-α and IFN-γ during inflammatory responses. In... |
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| SubjectTerms | Acute myeloid leukemia Adult Antibodies Blocking antibodies Cytokines Female Hepatitis A Virus Cellular Receptor 2 - immunology Humans Impact prediction Inflammation Interferon-gamma - genetics Interferon-gamma - immunology Interleukin 2 Intraepithelial Lymphocytes - immunology Leukemia Leukemia, Myeloid, Acute - immunology Lymphocytes Lymphocytes T Male Middle Aged Myeloid leukemia PD-1 PD-1 protein PD-L1 protein Programmed Cell Death 1 Receptor - immunology Stem cell transplantation Stem cells TIM-3 Transplantation Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - immunology Tumor necrosis factor-α Vδ2 T cell γ-Interferon |
| Title | Vδ2 T cell subsets, defined by PD-1 and TIM-3 expression, present varied cytokine responses in acute myeloid leukemia patients |
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