TIGIT Marks Exhausted T Cells, Correlates with Disease Progression, and Serves as a Target for Immune Restoration in HIV and SIV Infection
HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8+ T cells during HIV infection...
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| Published in | PLoS pathogens Vol. 12; no. 1; p. e1005349 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.01.2016
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
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| Abstract | HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8+ T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of TIGIT+ and TIGIT+ PD-1+ CD8+ T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific CD8+ T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific CD8+ T cell effector responses. The frequency of TIGIT+ CD4+ T cells correlated with the CD4+ T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion. |
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| AbstractList |
HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8+ T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of TIGIT+ and TIGIT+ PD-1+ CD8+ T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific CD8+ T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific CD8+ T cell effector responses. The frequency of TIGIT+ CD4+ T cells correlated with the CD4+ T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion. HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8+ T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of TIGIT+ and TIGIT+ PD-1+ CD8+ T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific CD8+ T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific CD8+ T cell effector responses. The frequency of TIGIT+ CD4+ T cells correlated with the CD4+ T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion. HIV infection induces phenotypic and functional changes to CD8 + T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8 + T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of TIGIT + and TIGIT + PD-1 + CD8 + T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific CD8 + T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific CD8 + T cell effector responses. The frequency of TIGIT + CD4 + T cells correlated with the CD4 + T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion. HIV-1 infection contributes substantially to global morbidity and mortality, with no immediate promise of an effective vaccine. One major obstacle to vaccine development and therapy is to understand why HIV-1 replication persists in a person despite the presence of viral specific immune responses. The emerging consensus has been that these immune cells are functionally ‘exhausted’ or anergic, and thus, although they can recognize HIV-1 specific target cells, they are unable to effectively keep up with rapid and dynamic viral replication in an individual. We have identified a novel combination pathway that can be targeted, TIGIT and PD-L1which may be responsible, at least in part, for making these immune cells dysfunctional and exhausted and thus unable to control the virus. We show that by blocking the TIGIT and PD-L1 pathway, we can reverse the defects of these viral specific immune cells. Our findings will give new directions to vaccines and therapies that will potentially reverse these dysfunctional cells and allow them to control HIV-1 replication, but also serve in “Shock and Kill” HIV curative strategies. HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8+ T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of TIGIT+ and TIGIT+ PD-1+ CD8+ T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific CD8+ T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific CD8+ T cell effector responses. The frequency of TIGIT+ CD4+ T cells correlated with the CD4+ T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion.HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector CD8+ T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of TIGIT+ and TIGIT+ PD-1+ CD8+ T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific CD8+ T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific CD8+ T cell effector responses. The frequency of TIGIT+ CD4+ T cells correlated with the CD4+ T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion. HIV infection induces phenotypic and functional changes to [CD8.sup.+] T cells defined by the coordinated upregulation of a series of negative checkpoint receptors that eventually result in T cell exhaustion and failure to control viral replication. We report that effector [CD8.sup.+] T cells during HIV infection in blood and SIV infection in lymphoid tissue exhibit higher levels of the negative checkpoint receptor TIGIT. Increased frequencies of [TIGIT.sup.+] and [TIGIT.sup.+] [PD-1.sup.+] [CD8.sup.+] T cells correlated with parameters of HIV and SIV disease progression. TIGIT remained elevated despite viral suppression in those with either pharmacological antiretroviral control or immunologically in elite controllers. HIV and SIV-specific [CD8.sup.+] T cells were dysfunctional and expressed high levels of TIGIT and PD-1. Ex-vivo single or combinational antibody blockade of TIGIT and/or PD-L1 restored viral-specific [CD8.sup.+] T cell effector responses. The frequency of [TIGIT.sup.+] [CD4.sup.+] T cells correlated with the [CD4.sup.+] T cell total HIV DNA. These findings identify TIGIT as a novel marker of dysfunctional HIV-specific T cells and suggest TIGIT along with other checkpoint receptors may be novel curative HIV targets to reverse T cell exhaustion. |
| Audience | Academic |
| Author | Mitchell, Brooks I. Sacha, Jonah B. Webb, Gabriela M. Hansen, Scott G. Maurer, Mark Deeks, Steven G. Ostrowski, Mario Ndhlovu, Lishomwa C. Ishii, Naoto Hecht, Frederick M. Chew, Glen M. Abdel-Mohsen, Mohamed Shikuma, Cecilia M. Fujita, Tsuyoshi Burwitz, Benjamin J. Reed, Jason S. Clayton, Kiera L. Liegler, Teri Hammond, Katherine B. Wu, Helen L. Korman, Alan J. |
| AuthorAffiliation | Emory University, UNITED STATES 1 Hawaii Center for HIV/AIDS, Department of Tropical Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii, United States of America 7 HIV/AIDS Division, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, California, United States of America 5 Department of Immunology, University of Toronto, Toronto, Ontario, Canada 4 Oregon National Primate Research Center, Oregon Health and Science University, Portland, Oregon, United States of America 6 Division of Experimental Medicine, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, California, United States of America 8 Biologics Discovery California, Bristol-Myers Squibb, Redwood City, California, United States of America 2 Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan 3 Vaccine and Gene Therapy Institute, Oregon |
| AuthorAffiliation_xml | – name: 8 Biologics Discovery California, Bristol-Myers Squibb, Redwood City, California, United States of America – name: 3 Vaccine and Gene Therapy Institute, Oregon Health and Science University, Portland, Oregon, United States of America – name: Emory University, UNITED STATES – name: 5 Department of Immunology, University of Toronto, Toronto, Ontario, Canada – name: 6 Division of Experimental Medicine, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, California, United States of America – name: 1 Hawaii Center for HIV/AIDS, Department of Tropical Medicine, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii, United States of America – name: 4 Oregon National Primate Research Center, Oregon Health and Science University, Portland, Oregon, United States of America – name: 7 HIV/AIDS Division, Department of Medicine, San Francisco General Hospital, University of California, San Francisco, San Francisco, California, United States of America – name: 2 Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan |
| Author_xml | – sequence: 1 givenname: Glen M. surname: Chew fullname: Chew, Glen M. – sequence: 2 givenname: Tsuyoshi surname: Fujita fullname: Fujita, Tsuyoshi – sequence: 3 givenname: Gabriela M. surname: Webb fullname: Webb, Gabriela M. – sequence: 4 givenname: Benjamin J. surname: Burwitz fullname: Burwitz, Benjamin J. – sequence: 5 givenname: Helen L. surname: Wu fullname: Wu, Helen L. – sequence: 6 givenname: Jason S. surname: Reed fullname: Reed, Jason S. – sequence: 7 givenname: Katherine B. surname: Hammond fullname: Hammond, Katherine B. – sequence: 8 givenname: Kiera L. surname: Clayton fullname: Clayton, Kiera L. – sequence: 9 givenname: Naoto surname: Ishii fullname: Ishii, Naoto – sequence: 10 givenname: Mohamed surname: Abdel-Mohsen fullname: Abdel-Mohsen, Mohamed – sequence: 11 givenname: Teri surname: Liegler fullname: Liegler, Teri – sequence: 12 givenname: Brooks I. surname: Mitchell fullname: Mitchell, Brooks I. – sequence: 13 givenname: Frederick M. surname: Hecht fullname: Hecht, Frederick M. – sequence: 14 givenname: Mario surname: Ostrowski fullname: Ostrowski, Mario – sequence: 15 givenname: Cecilia M. surname: Shikuma fullname: Shikuma, Cecilia M. – sequence: 16 givenname: Scott G. surname: Hansen fullname: Hansen, Scott G. – sequence: 17 givenname: Mark surname: Maurer fullname: Maurer, Mark – sequence: 18 givenname: Alan J. surname: Korman fullname: Korman, Alan J. – sequence: 19 givenname: Steven G. surname: Deeks fullname: Deeks, Steven G. – sequence: 20 givenname: Jonah B. surname: Sacha fullname: Sacha, Jonah B. – sequence: 21 givenname: Lishomwa C. surname: Ndhlovu fullname: Ndhlovu, Lishomwa C. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26741490$$D View this record in MEDLINE/PubMed |
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| Copyright | COPYRIGHT 2016 Public Library of Science 2016 Chew et al 2016 Chew et al 2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Chew GM, Fujita T, Webb GM, Burwitz BJ, Wu HL, Reed JS, et al. (2016) TIGIT Marks Exhausted T Cells, Correlates with Disease Progression, and Serves as a Target for Immune Restoration in HIV and SIV Infection. PLoS Pathog 12(1): e1005349. doi:10.1371/journal.ppat.1005349 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: GMC LCN JBS. Performed the experiments: GMC GMW TF BJB JSR HLW KBH BIM LCN JBS. Analyzed the data: GMC CMS KLC MO NI TL FMH MAM SGH MM AJK SGD JBS. Contributed reagents/materials/analysis tools: GMW BJB MM AJK KLC TF MAM. Wrote the paper: GMC CMS KLC MO NI TL FMH MAM SGH MM AJK SGD JBS LCN. I hereby declare that MM (Scientist, Immuno-Oncology) and AJK (Vice president, Immuno-Oncology) are employed by Bristol-Myers Squibb, and have no significant competing financial, professional or personal interests that might have influenced the performance or presentation of the work described in this manuscript. This does not alter our adherence to all PLOS Pathogens policies on sharing data and materials. JBS and LCN share equal co-senior authorship. |
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| Snippet | HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors... HIV infection induces phenotypic and functional changes to [CD8.sup.+] T cells defined by the coordinated upregulation of a series of negative checkpoint... HIV infection induces phenotypic and functional changes to CD8 + T cells defined by the coordinated upregulation of a series of negative checkpoint receptors... HIV infection induces phenotypic and functional changes to CD8+ T cells defined by the coordinated upregulation of a series of negative checkpoint receptors... |
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| SubjectTerms | Acquired immune deficiency syndrome AIDS Animals B7-H1 Antigen - immunology CD4-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - immunology Cell Separation Development and progression Disease Disease Progression DNA, Viral - analysis Flow Cytometry Funding Health aspects HIV HIV infection HIV Infections - immunology Host-virus relationships Human immunodeficiency virus Humans Immune response Infections Lymphocyte Activation - immunology Lymphocytes Macaca mulatta Mortality Observations Receptors, Immunologic - immunology RNA, Viral - analysis Simian Acquired Immunodeficiency Syndrome - immunology Simian immunodeficiency virus Statistical analysis T cells Viral infections |
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| Title | TIGIT Marks Exhausted T Cells, Correlates with Disease Progression, and Serves as a Target for Immune Restoration in HIV and SIV Infection |
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