Role of programmed death ligands in effective T-cell interactions in extranodal natural killer/T-cell lymphoma
Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative re...
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| Published in | Oncology letters Vol. 8; no. 4; pp. 1461 - 1469 |
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| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
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D.A. Spandidos
01.10.2014
Spandidos Publications Spandidos Publications UK Ltd |
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| Abstract | Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative regulatory signal. The current study analyzed the expression of programmed death 1 (PD-1)/programmed death ligand (PD-L) in ENKL cell lines and tissues. The functional studies were performed to analyze the functional activity of PD-L1 interacting with effective T cells in ENKL. PD-L1 and PD-L2 mRNA levels in ENKL cell lines were markedly upregulated compared with those in normal natural killer cells. The proteins constitutively expressed in the 30 ENKL specimens were significantly higher than in the 20 rhinitis specimens. In addition, PD-L1 and PD-L2 expression were found to closely correlate with certain clinical histopathological parameters. Furthermore, the count of PD-1+ tumor-infiltrating T lymphocytes was found to negatively correlate with the expression of PD-L1 and PD-L2. The PD-1 expression in the CD4+ and CD8+ T-cell subsets of 20 ENKL patients prior to therapy were significantly higher than that of the 10 healthy volunteers. In the functional studies, the cytokines (interleukin-2 and interferon-γ) secreted by CD8+ T cells were inhibited by PD-L1 expression in SNK-6 cells and this was restored with the presence of the PD-L1 blocking antibody. However no direct effect of PD-L1 was identified on CD8+ T-cell apoptosis and CD8+ T-cell cytotoxicity, as assessed by the proliferation of SNK-6 cells in the presence or absence of the neutralizing anti-PD-L1 antibody. The results of the current study revealed that PD-Ls and PD-1 are aberrantly expressed in ENKL and, furthermore, PD-L1 expression in SNK-6 cells was found to inhibit the activity of CD8+ T-cell cytokine secretion. This indicated that the PD-Ls may prevent effective antitumor immunity in vivo by interacting with tumor T cells, which provides important evidence to delineate the cellular immune deficiency mechanism in ENKL. Therefore, PD-1/PD-Ls are predicted to become novel targets for ENKL immunotherapy. |
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| AbstractList | Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative regulatory signal. The current study analyzed the expression of programmed death 1 (PD-1)/programmed death ligand (PD-L) in ENKL cell lines and tissues. The functional studies were performed to analyze the functional activity of PD-L1 interacting with effective T cells in ENKL. PD-L1 and PD-L2 mRNA levels in ENKL cell lines were markedly upregulated compared with those in normal natural killer cells. The proteins constitutively expressed in the 30 ENKL specimens were significantly higher than in the 20 rhinitis specimens. In addition, PD-L1 and PD-L2 expression were found to closely correlate with certain clinical histopathological parameters. Furthermore, the count of PD-1+ tumor-infiltrating T lymphocytes was found to negatively correlate with the expression of PD-L1 and PD-L2. The PD-1 expression in the CD4+ and CD8+ T-cell subsets of 20 ENKL patients prior to therapy were significantly higher than that of the 10 healthy volunteers. In the functional studies, the cytokines (interleukin-2 and interferon-γ) secreted by CD8+ T cells were inhibited by PD-L1 expression in SNK-6 cells and this was restored with the presence of the PD-L1 blocking antibody. However no direct effect of PD-L1 was identified on CD8+ T-cell apoptosis and CD8+ T-cell cytotoxicity, as assessed by the proliferation of SNK-6 cells in the presence or absence of the neutralizing anti-PD-L1 antibody. The results of the current study revealed that PD-Ls and PD-1 are aberrantly expressed in ENKL and, furthermore, PD-L1 expression in SNK-6 cells was found to inhibit the activity of CD8+ T-cell cytokine secretion. This indicated that the PD-Ls may prevent effective antitumor immunity in vivo by interacting with tumor T cells, which provides important evidence to delineate the cellular immune deficiency mechanism in ENKL. Therefore, PD-1/PD-Ls are predicted to become novel targets for ENKL immunotherapy. Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative regulatory signal. The current study analyzed the expression of programmed death 1 (PD-1)/programmed death ligand (PD-L) in ENKL cell lines and tissues. The functional studies were performed to analyze the functional activity of PD-L1 interacting with effective T cells in ENKL. PD-L1 and PD-L2 mRNA levels in ENKL cell lines were markedly upregulated compared with those in normal natural killer cells. The proteins constitutively expressed in the 30 ENKL specimens were significantly higher than in the 20 rhinitis specimens. In addition, PD-L1 and PD-L2 expression were found to closely correlate with certain clinical histopathological parameters. Furthermore, the count of PD-1 + tumor-infiltrating T lymphocytes was found to negatively correlate with the expression of PD-L1 and PD-L2. The PD-1 expression in the CD4 + and CD8 + T-cell subsets of 20 ENKL patients prior to therapy were significantly higher than that of the 10 healthy volunteers. In the functional studies, the cytokines (interleukin-2 and interferon-γ) secreted by CD8 + T cells were inhibited by PD-L1 expression in SNK-6 cells and this was restored with the presence of the PD-L1 blocking antibody. However no direct effect of PD-L1 was identified on CD8 + T-cell apoptosis and CD8 + T-cell cytotoxicity, as assessed by the proliferation of SNK-6 cells in the presence or absence of the neutralizing anti-PD-L1 antibody. The results of the current study revealed that PD-Ls and PD-1 are aberrantly expressed in ENKL and, furthermore, PD-L1 expression in SNK-6 cells was found to inhibit the activity of CD8 + T-cell cytokine secretion. This indicated that the PD-Ls may prevent effective antitumor immunity in vivo by interacting with tumor T cells, which provides important evidence to delineate the cellular immune deficiency mechanism in ENKL. Therefore, PD-1/PD-Ls are predicted to become novel targets for ENKL immunotherapy. Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative regulatory signal. The current study analyzed the expression of programmed death 1 (PD-1)/programmed death ligand (PD-L) in ENKL cell lines and tissues. The functional studies were performed to analyze the functional activity of PD-L1 interacting with effective T cells in ENKL. PD-L1 and PD-L2 mRNA levels in ENKL cell lines were markedly upregulated compared with those in normal natural killer cells. The proteins constitutively expressed in the 30 ENKL specimens were significantly higher than in the 20 rhinitis specimens. In addition, PD-L1 and PD-L2 expression were found to closely correlate with certain clinical histopathological parameters. Furthermore, the count of [PD-1.sup.+] tumor-infiltrating T lymphocytes was found to negatively correlate with the expression of PD-L1 and PD-L2. The PD-1 expression in the [CD4.sup.+] and [CD8.sup.+] T-cell subsets of 20 ENKL patients prior to therapy were significantly higher than that of the 10 healthy volunteers. In the functional studies, the cytokines (interleukin-2 and interferon-γ) secreted by [CD8.sup.+] T cells were inhibited by PD-L1 expression in SNK-6 cells and this was restored with the presence of the PD-L1 blocking antibody. However no direct effect of PD-L1 was identified on [CD8.sup.+] T-cell apoptosis and [CD8.sup.+] T-cell cytotoxicity, as assessed by the proliferation of SNK-6 cells in the presence or absence of the neutralizing anti-PD-L1 antibody. The results of the current study revealed that PD-Ls and PD-1 are aberrantly expressed in ENKL and, furthermore, PD-L1 expression in SNK-6 cells was found to inhibit the activity of [CD8.sup.+] T-cell cytokine secretion. This indicated that the PD-Ls may prevent effective antitumor immunity in vivo by interacting with tumor T cells, which provides important evidence to delineate the cellular immune deficiency mechanism in ENKL. Therefore, PD-1/PD-Ls are predicted to become novel targets for ENKL immunotherapy. Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative regulatory signal. The current study analyzed the expression of programmed death 1 (PD-1)/programmed death ligand (PD-L) in ENKL cell lines and tissues. The functional studies were performed to analyze the functional activity of PD-L1 interacting with effective T cells in ENKL. PD-L1 and PD-L2 mRNA levels in ENKL cell lines were markedly upregulated compared with those in normal natural killer cells. The proteins constitutively expressed in the 30 ENKL specimens were significantly higher than in the 20 rhinitis specimens. In addition, PD-L1 and PD-L2 expression were found to closely correlate with certain clinical histopathological parameters. Furthermore, the count of [PD-1.sup.+] tumor-infiltrating T lymphocytes was found to negatively correlate with the expression of PD-L1 and PD-L2. The PD-1 expression in the [CD4.sup.+] and [CD8.sup.+] T-cell subsets of 20 ENKL patients prior to therapy were significantly higher than that of the 10 healthy volunteers. In the functional studies, the cytokines (interleukin-2 and interferon-γ) secreted by [CD8.sup.+] T cells were inhibited by PD-L1 expression in SNK-6 cells and this was restored with the presence of the PD-L1 blocking antibody. However no direct effect of PD-L1 was identified on [CD8.sup.+] T-cell apoptosis and [CD8.sup.+] T-cell cytotoxicity, as assessed by the proliferation of SNK-6 cells in the presence or absence of the neutralizing anti-PD-L1 antibody. The results of the current study revealed that PD-Ls and PD-1 are aberrantly expressed in ENKL and, furthermore, PD-L1 expression in SNK-6 cells was found to inhibit the activity of [CD8.sup.+] T-cell cytokine secretion. This indicated that the PD-Ls may prevent effective antitumor immunity in vivo by interacting with tumor T cells, which provides important evidence to delineate the cellular immune deficiency mechanism in ENKL. Therefore, PD-1/PD-Ls are predicted to become novel targets for ENKL immunotherapy. Key words: programmed death 1 ligand, B7 family, lymphoma, programmed death 2 ligand, programmed cell death 1, natural killer/T cell Extranodal natural killer/T-cell lymphoma (ENKL) is marked by a profound cellular immune deficiency that may influence the capacity of T cells to extract an efficient antitumor immune response. It has been confirmed that the B7-CD28 pathway may promote tumor immune evasion by providing a negative regulatory signal. The current study analyzed the expression of programmed death 1 (PD-1)/programmed death ligand (PD-L) in ENKL cell lines and tissues. The functional studies were performed to analyze the functional activity of PD-L1 interacting with effective T cells in ENKL. PD-L1 and PD-L2 mRNA levels in ENKL cell lines were markedly upregulated compared with those in normal natural killer cells. The proteins constitutively expressed in the 30 ENKL specimens were significantly higher than in the 20 rhinitis specimens. In addition, PD-L1 and PD-L2 expression were found to closely correlate with certain clinical histopathological parameters. Furthermore, the count of PD-1 tumor-infiltrating T lymphocytes was found to negatively correlate with the expression of PD-L1 and PD-L2. The PD-1 expression in the CD4 and CD8 T-cell subsets of 20 ENKL patients prior to therapy were significantly higher than that of the 10 healthy volunteers. In the functional studies, the cytokines (interleukin-2 and interferon-γ) secreted by CD8 T cells were inhibited by PD-L1 expression in SNK-6 cells and this was restored with the presence of the PD-L1 blocking antibody. However no direct effect of PD-L1 was identified on CD8 T-cell apoptosis and CD8 T-cell cytotoxicity, as assessed by the proliferation of SNK-6 cells in the presence or absence of the neutralizing anti-PD-L1 antibody. The results of the current study revealed that PD-Ls and PD-1 are aberrantly expressed in ENKL and, furthermore, PD-L1 expression in SNK-6 cells was found to inhibit the activity of CD8 T-cell cytokine secretion. This indicated that the PD-Ls may prevent effective antitumor immunity by interacting with tumor T cells, which provides important evidence to delineate the cellular immune deficiency mechanism in ENKL. Therefore, PD-1/PD-Ls are predicted to become novel targets for ENKL immunotherapy. |
| Audience | Academic |
| Author | LIU, FEIFEI WEN, JIANGUO CHEN, XINFENG SUN, SUKE ZHANG, XUDONG ZHANG, MINGZHI LI, RUPING HU, TENGPENG LI, ZHAOMING HAN, LIJUAN YOUNG, KEN ZHOU, ZHIYUAN ZHANG, YI |
| AuthorAffiliation | 2 Department of Sports Medicine, Research Center of Sports Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China 5 Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China 3 Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China 1 Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China 4 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77230-1439, USA |
| AuthorAffiliation_xml | – name: 2 Department of Sports Medicine, Research Center of Sports Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China – name: 5 Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – name: 4 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77230-1439, USA – name: 1 Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – name: 3 Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China |
| Author_xml | – sequence: 1 givenname: LIJUAN surname: HAN fullname: HAN, LIJUAN organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 2 givenname: FEIFEI surname: LIU fullname: LIU, FEIFEI organization: Department of Sports Medicine, Research Center of Sports Medicine, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China – sequence: 3 givenname: RUPING surname: LI fullname: LI, RUPING organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 4 givenname: ZHAOMING surname: LI fullname: LI, ZHAOMING organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 5 givenname: XINFENG surname: CHEN fullname: CHEN, XINFENG organization: Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 6 givenname: ZHIYUAN surname: ZHOU fullname: ZHOU, ZHIYUAN organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 7 givenname: XUDONG surname: ZHANG fullname: ZHANG, XUDONG organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 8 givenname: TENGPENG surname: HU fullname: HU, TENGPENG organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 9 givenname: YI surname: ZHANG fullname: ZHANG, YI organization: Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 10 givenname: KEN surname: YOUNG fullname: YOUNG, KEN organization: Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77230-1439, USA – sequence: 11 givenname: SUKE surname: SUN fullname: SUN, SUKE organization: Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 12 givenname: JIANGUO surname: WEN fullname: WEN, JIANGUO organization: Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China – sequence: 13 givenname: MINGZHI surname: ZHANG fullname: ZHANG, MINGZHI organization: Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25202350$$D View this record in MEDLINE/PubMed |
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| Keywords | natural killer/T cell programmed death 2 ligand B7 family programmed cell death 1 programmed death 1 ligand lymphoma |
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| SubjectTerms | Age B7 family Care and treatment Cell death Cellular biology Chemotherapy Classification Cytokines Hospitals Immune response Immunotherapy Innovations Leukemia Ligands Lymphocytes Lymphoma Males natural killer/T cell Oncology programmed cell death 1 programmed death 1 ligand programmed death 2 ligand Regulation Science Studies T cell lymphoma T cell receptors Tumors |
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| Title | Role of programmed death ligands in effective T-cell interactions in extranodal natural killer/T-cell lymphoma |
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