TIGIT enhances CD4+ regulatory T‐cell response and mediates immune suppression in a murine ovarian cancer model

Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TI...

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Published inCancer medicine (Malden, MA) Vol. 9; no. 10; pp. 3584 - 3591
Main Authors Chen, Fengzhen, Xu, Yanying, Chen, Yulong, Shan, Shu
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.05.2020
John Wiley and Sons Inc
Wiley
Subjects
Antibodies
Apoptosis
Ascites
Cancer Biology
Cancer therapies
CD4 antigen
CD8 antigen
Cell activation
Chemotherapy
Cloning
Enzymes
Experiments
Flow cytometry
Immune checkpoint
Immunoglobulins
Immunoregulation
Immunosuppression
Laboratory animals
Lymphocytes
Lymphocytes T
Medical prognosis
Monoclonal antibodies
Natural killer cells
Original Research
Ovarian cancer
regulatory T cell
Spleen
Therapeutic applications
TIGIT
Tumors
immunosuppression
regulatory T cell
TIGIT
ovarian cancer
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Abstract Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4+ Tregs. Anti‐TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti‐TIGIT treatment reduced the proportion of CD4+ Tregs, but did not affect CD4+ and CD8+ T cells or natural killer cells. Splenic CD4+ Tregs from OC mice were isolated after the anti‐TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4+ Tregs. A survival curve suggested that anti‐TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4+ Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients. TIGIT enhanced CD4+ Tregs response and mediated immune suppression in OC; TIGIT is a potential target in OC patients.
AbstractList Abstract Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4+ Tregs. Anti‐TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti‐TIGIT treatment reduced the proportion of CD4+ Tregs, but did not affect CD4+ and CD8+ T cells or natural killer cells. Splenic CD4+ Tregs from OC mice were isolated after the anti‐TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4+ Tregs. A survival curve suggested that anti‐TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4+ Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients.
Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4+ Tregs. Anti‐TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti‐TIGIT treatment reduced the proportion of CD4+ Tregs, but did not affect CD4+ and CD8+ T cells or natural killer cells. Splenic CD4+ Tregs from OC mice were isolated after the anti‐TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4+ Tregs. A survival curve suggested that anti‐TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4+ Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients.
Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4+ Tregs. Anti‐TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti‐TIGIT treatment reduced the proportion of CD4+ Tregs, but did not affect CD4+ and CD8+ T cells or natural killer cells. Splenic CD4+ Tregs from OC mice were isolated after the anti‐TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4+ Tregs. A survival curve suggested that anti‐TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4+ Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients. TIGIT enhanced CD4+ Tregs response and mediated immune suppression in OC; TIGIT is a potential target in OC patients.
Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4 + Tregs. Anti‐TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti‐TIGIT treatment reduced the proportion of CD4 + Tregs, but did not affect CD4 + and CD8 + T cells or natural killer cells. Splenic CD4 + Tregs from OC mice were isolated after the anti‐TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4 + Tregs. A survival curve suggested that anti‐TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4 + Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients.
Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T‐cell immunoglobulin and ITIM domain (TIGIT) is a well‐known immune checkpoint molecule that inhibits T‐cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4 + Tregs. Anti‐TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti‐TIGIT treatment reduced the proportion of CD4 + Tregs, but did not affect CD4 + and CD8 + T cells or natural killer cells. Splenic CD4 + Tregs from OC mice were isolated after the anti‐TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4 + Tregs. A survival curve suggested that anti‐TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4 + Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients. TIGIT enhanced CD4 + Tregs response and mediated immune suppression in OC; TIGIT is a potential target in OC patients.
Ovarian cancer (OC) is the fifth-leading cause of cancer-related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T-cell immunoglobulin and ITIM domain (TIGIT) is a well-known immune checkpoint molecule that inhibits T-cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4+ Tregs. Anti-TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti-TIGIT treatment reduced the proportion of CD4+ Tregs, but did not affect CD4+ and CD8+ T cells or natural killer cells. Splenic CD4+ Tregs from OC mice were isolated after the anti-TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4+ Tregs. A survival curve suggested that anti-TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4+ Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients.Ovarian cancer (OC) is the fifth-leading cause of cancer-related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T-cell immunoglobulin and ITIM domain (TIGIT) is a well-known immune checkpoint molecule that inhibits T-cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4+ Tregs. Anti-TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti-TIGIT treatment reduced the proportion of CD4+ Tregs, but did not affect CD4+ and CD8+ T cells or natural killer cells. Splenic CD4+ Tregs from OC mice were isolated after the anti-TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4+ Tregs. A survival curve suggested that anti-TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4+ Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients.
Ovarian cancer (OC) is the fifth-leading cause of cancer-related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The T-cell immunoglobulin and ITIM domain (TIGIT) is a well-known immune checkpoint molecule that inhibits T-cell responses. However, the role of TIGIT in OC is not comprehensively understood. In this study, we revealed crucial functions of TIGIT in the development and progression of OC. ID8 cells were used to establish a murine OC model. TIGIT expression was increased in immune cells of OC mice, particularly in CD4 Tregs. Anti-TIGIT monoclonal antibodies (mAb) were used to block the function of TIGIT in OC mice, and we found that the anti-TIGIT treatment reduced the proportion of CD4 Tregs, but did not affect CD4 and CD8 T cells or natural killer cells. Splenic CD4 Tregs from OC mice were isolated after the anti-TIGIT treatment, and their functioning was examined. Inhibition of TIGIT lowered the degree of immunosuppression induced by CD4 Tregs. A survival curve suggested that anti-TIGIT treatment can improve the survival rate of OC in mice. We conclude that TIGIT enhanced CD4 Tregs response and mediated immunosuppression in the OC model. Our data suggest that inhibition of TIGIT is a potential therapeutic target in OC patients.
Author Xu, Yanying
Chen, Yulong
Shan, Shu
Chen, Fengzhen
AuthorAffiliation 2 Department of Lung Oncology Tianjin Medical University Cancer Institute and Hospital Tianjin China
3 Department of Gynecology and Obstetrics Affiliated Tongji Hospital Tongji University Shanghai China
1 Department of Gynecology The Second Hospital of Tianjin Medical University Tianjin China
AuthorAffiliation_xml – name: 2 Department of Lung Oncology Tianjin Medical University Cancer Institute and Hospital Tianjin China
– name: 3 Department of Gynecology and Obstetrics Affiliated Tongji Hospital Tongji University Shanghai China
– name: 1 Department of Gynecology The Second Hospital of Tianjin Medical University Tianjin China
Author_xml – sequence: 1
  givenname: Fengzhen
  orcidid: 0000-0002-1205-4714
  surname: Chen
  fullname: Chen, Fengzhen
  email: cfz_blue_7@163.com
  organization: The Second Hospital of Tianjin Medical University
– sequence: 2
  givenname: Yanying
  surname: Xu
  fullname: Xu, Yanying
  organization: The Second Hospital of Tianjin Medical University
– sequence: 3
  givenname: Yulong
  surname: Chen
  fullname: Chen, Yulong
  organization: Tianjin Medical University Cancer Institute and Hospital
– sequence: 4
  givenname: Shu
  surname: Shan
  fullname: Shan, Shu
  organization: Tongji University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32212317$$D View this record in MEDLINE/PubMed
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Issue 10
Keywords immunosuppression
regulatory T cell
TIGIT
ovarian cancer
Language English
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This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Snippet Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The...
Ovarian cancer (OC) is the fifth-leading cause of cancer-related death in women with a pathogenesis involving activation of regulatory T cells (Tregs). The...
Abstract Ovarian cancer (OC) is the fifth‐leading cause of cancer‐related death in women with a pathogenesis involving activation of regulatory T cells...
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SubjectTerms Antibodies
Apoptosis
Ascites
Cancer Biology
Cancer therapies
CD4 antigen
CD8 antigen
Cell activation
Chemotherapy
Cloning
Enzymes
Experiments
Flow cytometry
Immune checkpoint
Immunoglobulins
Immunoregulation
Immunosuppression
Laboratory animals
Lymphocytes
Lymphocytes T
Medical prognosis
Monoclonal antibodies
Natural killer cells
Original Research
Ovarian cancer
regulatory T cell
Spleen
Therapeutic applications
TIGIT
Tumors
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Title TIGIT enhances CD4+ regulatory T‐cell response and mediates immune suppression in a murine ovarian cancer model
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fcam4.2976
https://www.ncbi.nlm.nih.gov/pubmed/32212317
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Volume 9
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