Hyper-Expression of PD-1 Is Associated with the Levels of Exhausted and Dysfunctional Phenotypes of Circulating CD161++TCR iVα7.2+ Mucosal-Associated Invariant T Cells in Chronic Hepatitis B Virus Infection
Mucosal-associated invariant T (MAIT) cells, defined as CD161 TCR iVα7.2 T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chron...
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| Published in | Frontiers in immunology Vol. 9; p. 472 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers Media S.A
19.03.2018
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| Subjects | |
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| Abstract | Mucosal-associated invariant T (MAIT) cells, defined as CD161
TCR iVα7.2
T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chronic hepatitis B virus (HBV) infection. The peripheral CD3
CD161
TCR iVα7.2
MAIT cells in chronic HBV-infected patients and healthy controls were phenotypically characterized based on CD57, PD-1, TIM-3, and CTLA-4, as well as HLA-DR and CD38 expression. The frequency of MAIT cells was significantly decreased among chronic HBV-infected individuals as compared to controls. Expression of CD57, PD-1, CTLA-4, as well as HLA-DR and CD38 on MAIT cells was significantly elevated in chronic HBV-infected individuals relative to controls. The percentage of T cell receptor (TCR) iVα7.2
CD161
MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4
T cells and MAIT cells and with CD57 on CD8
T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation. The percentage and expression levels of PD-1 as well as CTLA-4 on MAIT cells inversely correlated with plasma HBV-DNA levels, which may suggest either a role for MAIT cells in the control of HBV infection or the effect of HBV replication in the liver on MAIT cell phenotype. We report that decrease of TCR iVα7.2
MAIT cells in the peripheral blood and their functions were seemingly impaired in chronic HBV-infected patients likely because of the increased expression of PD-1. |
|---|---|
| AbstractList | Mucosal-associated invariant T (MAIT) cells, defined as CD161
++
TCR iVα7.2
+
T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chronic hepatitis B virus (HBV) infection. The peripheral CD3
+
CD161
++
TCR iVα7.2
+
MAIT cells in chronic HBV-infected patients and healthy controls were phenotypically characterized based on CD57, PD-1, TIM-3, and CTLA-4, as well as HLA-DR and CD38 expression. The frequency of MAIT cells was significantly decreased among chronic HBV-infected individuals as compared to controls. Expression of CD57, PD-1, CTLA-4, as well as HLA-DR and CD38 on MAIT cells was significantly elevated in chronic HBV-infected individuals relative to controls. The percentage of T cell receptor (TCR) iVα7.2
+
CD161
+
MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4
+
T cells and MAIT cells and with CD57 on CD8
+
T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation. The percentage and expression levels of PD-1 as well as CTLA-4 on MAIT cells inversely correlated with plasma HBV-DNA levels, which may suggest either a role for MAIT cells in the control of HBV infection or the effect of HBV replication in the liver on MAIT cell phenotype. We report that decrease of TCR iVα7.2
+
MAIT cells in the peripheral blood and their functions were seemingly impaired in chronic HBV-infected patients likely because of the increased expression of PD-1. Mucosal-associated invariant T (MAIT) cells, defined as CD161++TCR iVα7.2+ T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chronic hepatitis B virus (HBV) infection. The peripheral CD3+CD161++TCR iVα7.2+ MAIT cells in chronic HBV-infected patients and healthy controls were phenotypically characterized based on CD57, PD-1, TIM-3, and CTLA-4, as well as HLA-DR and CD38 expression. The frequency of MAIT cells was significantly decreased among chronic HBV-infected individuals as compared to controls. Expression of CD57, PD-1, CTLA-4, as well as HLA-DR and CD38 on MAIT cells was significantly elevated in chronic HBV-infected individuals relative to controls. The percentage of T cell receptor (TCR) iVα7.2+ CD161+ MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4+ T cells and MAIT cells and with CD57 on CD8+ T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation. The percentage and expression levels of PD-1 as well as CTLA-4 on MAIT cells inversely correlated with plasma HBV-DNA levels, which may suggest either a role for MAIT cells in the control of HBV infection or the effect of HBV replication in the liver on MAIT cell phenotype. We report that decrease of TCR iVα7.2+ MAIT cells in the peripheral blood and their functions were seemingly impaired in chronic HBV-infected patients likely because of the increased expression of PD-1.Mucosal-associated invariant T (MAIT) cells, defined as CD161++TCR iVα7.2+ T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chronic hepatitis B virus (HBV) infection. The peripheral CD3+CD161++TCR iVα7.2+ MAIT cells in chronic HBV-infected patients and healthy controls were phenotypically characterized based on CD57, PD-1, TIM-3, and CTLA-4, as well as HLA-DR and CD38 expression. The frequency of MAIT cells was significantly decreased among chronic HBV-infected individuals as compared to controls. Expression of CD57, PD-1, CTLA-4, as well as HLA-DR and CD38 on MAIT cells was significantly elevated in chronic HBV-infected individuals relative to controls. The percentage of T cell receptor (TCR) iVα7.2+ CD161+ MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4+ T cells and MAIT cells and with CD57 on CD8+ T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation. The percentage and expression levels of PD-1 as well as CTLA-4 on MAIT cells inversely correlated with plasma HBV-DNA levels, which may suggest either a role for MAIT cells in the control of HBV infection or the effect of HBV replication in the liver on MAIT cell phenotype. We report that decrease of TCR iVα7.2+ MAIT cells in the peripheral blood and their functions were seemingly impaired in chronic HBV-infected patients likely because of the increased expression of PD-1. Mucosal-associated invariant T (MAIT) cells, defined as CD161++TCR iVα7.2+ T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chronic hepatitis B virus (HBV) infection. The peripheral CD3+CD161++TCR iVα7.2+ MAIT cells in chronic HBV-infected patients and healthy controls were phenotypically characterized based on CD57, PD-1, TIM-3, and CTLA-4, as well as HLA-DR and CD38 expression. The frequency of MAIT cells was significantly decreased among chronic HBV-infected individuals as compared to controls. Expression of CD57, PD-1, CTLA-4, as well as HLA-DR and CD38 on MAIT cells was significantly elevated in chronic HBV-infected individuals relative to controls. The percentage of T cell receptor (TCR) iVα7.2+ CD161+ MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4+ T cells and MAIT cells and with CD57 on CD8+ T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation. The percentage and expression levels of PD-1 as well as CTLA-4 on MAIT cells inversely correlated with plasma HBV-DNA levels, which may suggest either a role for MAIT cells in the control of HBV infection or the effect of HBV replication in the liver on MAIT cell phenotype. We report that decrease of TCR iVα7.2+ MAIT cells in the peripheral blood and their functions were seemingly impaired in chronic HBV-infected patients likely because of the increased expression of PD-1. Mucosal-associated invariant T (MAIT) cells, defined as CD161 TCR iVα7.2 T cells, play an important role in the innate defense against bacterial infections, and their functionality is impaired in chronic viral infections. Here, we investigated the frequency and functional role of MAIT cells in chronic hepatitis B virus (HBV) infection. The peripheral CD3 CD161 TCR iVα7.2 MAIT cells in chronic HBV-infected patients and healthy controls were phenotypically characterized based on CD57, PD-1, TIM-3, and CTLA-4, as well as HLA-DR and CD38 expression. The frequency of MAIT cells was significantly decreased among chronic HBV-infected individuals as compared to controls. Expression of CD57, PD-1, CTLA-4, as well as HLA-DR and CD38 on MAIT cells was significantly elevated in chronic HBV-infected individuals relative to controls. The percentage of T cell receptor (TCR) iVα7.2 CD161 MAIT cells did not correlate with HBV viral load but inversely with HLA-DR on CD4 T cells and MAIT cells and with CD57 on CD8 T cells suggesting that decrease of MAIT cells may not be attributed to direct infection by HBV but driven by HBV-induced chronic immune activation. The percentage and expression levels of PD-1 as well as CTLA-4 on MAIT cells inversely correlated with plasma HBV-DNA levels, which may suggest either a role for MAIT cells in the control of HBV infection or the effect of HBV replication in the liver on MAIT cell phenotype. We report that decrease of TCR iVα7.2 MAIT cells in the peripheral blood and their functions were seemingly impaired in chronic HBV-infected patients likely because of the increased expression of PD-1. |
| Author | Murugesan, Amudhan Vadivelu, Jamuna Velu, Vijayakumar Ansari, Abdul W. Batran, Rami Al Vignesh, Ramachandran Shankar, Esaki M. Tan, Hong Y. Larsson, Marie Enström, Philip F. Chattopadhyay, Indranil Ussher, James E. Rajarajeswaran, Jayakumar Kamarulzaman, Adeeba Saeidi, Alireza Rosmawati, Mohamed Vasuki, V. Yong, Yean K. |
| AuthorAffiliation | 1 Laboratory Center, Xiamen University Malaysia , Sepang , Malaysia 14 Department of Microbiology and Immunology, Emory Vaccine Center , Atlanta, GA , United States 9 The Government Theni Medical College and Hospital , Theni , India 15 Division of Infection Biology, Department of Life Sciences, Central University of Tamil Nadu , Thiruvarur , India 10 Laboratory-Based Department, Universiti Kuala Lumpur , Ipoh , Malaysia 3 China-ASEAN Institute of Marine Science (CAMS), Xiamen University Malaysia , Sepang , Malaysia 7 Department of Microbiology, The Government Thiruvarur Medical College and Hospital , Thiruvarur , India 11 Center of Excellence for Research in AIDS, University of Malaya , Kuala Lumpur , Malaysia 2 Department of Medicine, University of Malaya Medical Centre , Kuala Lumpur , Malaysia 4 Department of Traditional Chinese Medicine, Xiamen University Malaysia , Sepang , Malaysia 12 Department of Molecular Medicine, Faculty of Medicine, University of Malaya , Kuala Lumpur , Malaysia 6 Dep |
| AuthorAffiliation_xml | – name: 4 Department of Traditional Chinese Medicine, Xiamen University Malaysia , Sepang , Malaysia – name: 6 Department of Medical Microbiology, Faculty of Medicine, University of Malaya , Kuala Lumpur , Malaysia – name: 8 Division of Molecular Cancer Biology, Department of Life Sciences, Central University of Tamil Nadu , Thiruvarur , India – name: 3 China-ASEAN Institute of Marine Science (CAMS), Xiamen University Malaysia , Sepang , Malaysia – name: 10 Laboratory-Based Department, Universiti Kuala Lumpur , Ipoh , Malaysia – name: 5 Division of Molecular Virology, Department of Clinical and Experimental Medicine, Linköping University , Linköping , Sweden – name: 14 Department of Microbiology and Immunology, Emory Vaccine Center , Atlanta, GA , United States – name: 12 Department of Molecular Medicine, Faculty of Medicine, University of Malaya , Kuala Lumpur , Malaysia – name: 15 Division of Infection Biology, Department of Life Sciences, Central University of Tamil Nadu , Thiruvarur , India – name: 1 Laboratory Center, Xiamen University Malaysia , Sepang , Malaysia – name: 7 Department of Microbiology, The Government Thiruvarur Medical College and Hospital , Thiruvarur , India – name: 11 Center of Excellence for Research in AIDS, University of Malaya , Kuala Lumpur , Malaysia – name: 16 Department of Microbiology, Central University of Tamil Nadu , Thiruvarur , India – name: 13 Department of Microbiology and Immunology, University of Otago , Dunedin , New Zealand – name: 2 Department of Medicine, University of Malaya Medical Centre , Kuala Lumpur , Malaysia – name: 9 The Government Theni Medical College and Hospital , Theni , India |
| Author_xml | – sequence: 1 givenname: Yean K. surname: Yong fullname: Yong, Yean K. – sequence: 2 givenname: Alireza surname: Saeidi fullname: Saeidi, Alireza – sequence: 3 givenname: Hong Y. surname: Tan fullname: Tan, Hong Y. – sequence: 4 givenname: Mohamed surname: Rosmawati fullname: Rosmawati, Mohamed – sequence: 5 givenname: Philip F. surname: Enström fullname: Enström, Philip F. – sequence: 6 givenname: Rami Al surname: Batran fullname: Batran, Rami Al – sequence: 7 givenname: V. surname: Vasuki fullname: Vasuki, V. – sequence: 8 givenname: Indranil surname: Chattopadhyay fullname: Chattopadhyay, Indranil – sequence: 9 givenname: Amudhan surname: Murugesan fullname: Murugesan, Amudhan – sequence: 10 givenname: Ramachandran surname: Vignesh fullname: Vignesh, Ramachandran – sequence: 11 givenname: Adeeba surname: Kamarulzaman fullname: Kamarulzaman, Adeeba – sequence: 12 givenname: Jayakumar surname: Rajarajeswaran fullname: Rajarajeswaran, Jayakumar – sequence: 13 givenname: Abdul W. surname: Ansari fullname: Ansari, Abdul W. – sequence: 14 givenname: Jamuna surname: Vadivelu fullname: Vadivelu, Jamuna – sequence: 15 givenname: James E. surname: Ussher fullname: Ussher, James E. – sequence: 16 givenname: Vijayakumar surname: Velu fullname: Velu, Vijayakumar – sequence: 17 givenname: Marie surname: Larsson fullname: Larsson, Marie – sequence: 18 givenname: Esaki M. surname: Shankar fullname: Shankar, Esaki M. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29616020$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2018 Yong, Saeidi, Tan, Rosmawati, Enström, Batran, Vasuki, Chattopadhyay, Murugesan, Vignesh, Kamarulzaman, Rajarajeswaran, Ansari, Vadivelu, Ussher, Velu, Larsson and Shankar. 2018 Yong, Saeidi, Tan, Rosmawati, Enström, Batran, Vasuki, Chattopadhyay, Murugesan, Vignesh, Kamarulzaman, Rajarajeswaran, Ansari, Vadivelu, Ussher, Velu, Larsson and Shankar |
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| Keywords | immunosenescence HLA-DR HBV infection mucosal-associated invariant T cells CTLA-4 immune exhaustion PD-1 |
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| Snippet | Mucosal-associated invariant T (MAIT) cells, defined as CD161
TCR iVα7.2
T cells, play an important role in the innate defense against bacterial infections,... Mucosal-associated invariant T (MAIT) cells, defined as CD161++TCR iVα7.2+ T cells, play an important role in the innate defense against bacterial infections,... Mucosal-associated invariant T (MAIT) cells, defined as CD161 ++ TCR iVα7.2 + T cells, play an important role in the innate defense against bacterial... |
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| SubjectTerms | HBV infection HLA-DR immune exhaustion Immunology immunosenescence mucosal-associated invariant T cells PD-1 |
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| Title | Hyper-Expression of PD-1 Is Associated with the Levels of Exhausted and Dysfunctional Phenotypes of Circulating CD161++TCR iVα7.2+ Mucosal-Associated Invariant T Cells in Chronic Hepatitis B Virus Infection |
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