Evidence of potent humoral immune activity in COVID‐19‐infected kidney transplant recipients
Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surf...
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| Published in | American journal of transplantation Vol. 20; no. 11; pp. 3149 - 3161 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Limited
01.11.2020
John Wiley and Sons Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID‐19) infection and 36 matched, transplanted controls without COVID‐19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4+ and CD8+ T cells in the COVID‐19 subjects. We also showed fewer anergic and senescent CD8+ T cells in COVID‐19 individuals, but no differences in exhausted CD8+ T cells, nor in any of these CD4+ T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID‐19 patients. Sixteen of 18 COVID‐19 subjects tested for anti‐SARS‐CoV‐2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID‐19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID‐19 infection can mount SARS‐CoV‐2‐reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID‐19 may not be required.
Hospitalized kidney transplant recipients with COVID‐19 infection can mount anti‐SARS‐CoV‐2–adaptive immune responses, despite ongoing immunosuppression, raising the possibility that empiric reduction of immunosuppression may not be required. |
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| AbstractList | Whether kidney transplant recipients are capable of mounting an effective anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID-19) infection and 36 matched, transplanted controls without COVID-19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4
and CD8
T cells in the COVID-19 subjects. We also showed fewer anergic and senescent CD8
T cells in COVID-19 individuals, but no differences in exhausted CD8
T cells, nor in any of these CD4
T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID-19 patients. Sixteen of 18 COVID-19 subjects tested for anti-SARS-CoV-2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID-19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID-19 infection can mount SARS-CoV-2-reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID-19 may not be required. Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID‐19) infection and 36 matched, transplanted controls without COVID‐19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4 + and CD8 + T cells in the COVID‐19 subjects. We also showed fewer anergic and senescent CD8 + T cells in COVID‐19 individuals, but no differences in exhausted CD8 + T cells, nor in any of these CD4 + T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID‐19 patients. Sixteen of 18 COVID‐19 subjects tested for anti‐SARS‐CoV‐2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID‐19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID‐19 infection can mount SARS‐CoV‐2‐reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID‐19 may not be required. Hospitalized kidney transplant recipients with COVID‐19 infection can mount anti‐SARS‐CoV‐2–adaptive immune responses, despite ongoing immunosuppression, raising the possibility that empiric reduction of immunosuppression may not be required. Whether kidney transplant recipients are capable of mounting an effective anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID-19) infection and 36 matched, transplanted controls without COVID-19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4+ and CD8+ T cells in the COVID-19 subjects. We also showed fewer anergic and senescent CD8+ T cells in COVID-19 individuals, but no differences in exhausted CD8+ T cells, nor in any of these CD4+ T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID-19 patients. Sixteen of 18 COVID-19 subjects tested for anti-SARS-CoV-2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID-19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID-19 infection can mount SARS-CoV-2-reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID-19 may not be required.Whether kidney transplant recipients are capable of mounting an effective anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID-19) infection and 36 matched, transplanted controls without COVID-19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4+ and CD8+ T cells in the COVID-19 subjects. We also showed fewer anergic and senescent CD8+ T cells in COVID-19 individuals, but no differences in exhausted CD8+ T cells, nor in any of these CD4+ T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID-19 patients. Sixteen of 18 COVID-19 subjects tested for anti-SARS-CoV-2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID-19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID-19 infection can mount SARS-CoV-2-reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID-19 may not be required. Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID‐19) infection and 36 matched, transplanted controls without COVID‐19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4+ and CD8+ T cells in the COVID‐19 subjects. We also showed fewer anergic and senescent CD8+ T cells in COVID‐19 individuals, but no differences in exhausted CD8+ T cells, nor in any of these CD4+ T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID‐19 patients. Sixteen of 18 COVID‐19 subjects tested for anti‐SARS‐CoV‐2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID‐19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID‐19 infection can mount SARS‐CoV‐2‐reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID‐19 may not be required. Hospitalized kidney transplant recipients with COVID‐19 infection can mount anti‐SARS‐CoV‐2–adaptive immune responses, despite ongoing immunosuppression, raising the possibility that empiric reduction of immunosuppression may not be required. Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune response despite chronic immunosuppression is unknown and has important implications for therapy. Herein, we analyzed peripheral blood cell surface and intracellular cytokine phenotyping by flow cytometry along with serum antibody testing in 18 kidney transplant recipients with active coronavirus disease 2019 (COVID‐19) infection and 36 matched, transplanted controls without COVID‐19. We observed significantly fewer total lymphocytes and fewer circulating memory CD4+ and CD8+ T cells in the COVID‐19 subjects. We also showed fewer anergic and senescent CD8+ T cells in COVID‐19 individuals, but no differences in exhausted CD8+ T cells, nor in any of these CD4+ T cell subsets between groups. We also observed greater frequencies of activated B cells in the COVID‐19 patients. Sixteen of 18 COVID‐19 subjects tested for anti‐SARS‐CoV‐2 serum antibodies showed positive immunoglobulin M or immunoglobulin G titers. Additional analyses showed no significant correlation among immune phenotypes and degrees of COVID‐19 disease severity. Our findings indicate that immunosuppressed kidney transplant recipients admitted to the hospital with acute COVID‐19 infection can mount SARS‐CoV‐2‐reactive adaptive immune responses. The findings raise the possibility that empiric reductions in immunosuppressive therapy for all kidney transplant recipients with active COVID‐19 may not be required. |
| Author | Leech, John M. Hartzell, Susan Benedetti, Claudia Florman, Sander Zaza, Gianluigi Riella, Leonardo V. Menon, Madhav C. Rahman, Adeeb H. Bin, Sofia Gallon, Lorenzo Cravedi, Paolo Haverly, Meredith Heeger, Peter S. |
| AuthorAffiliation | 3 Renal Unit Department of Medicine University Hospital of Verona Verona Italy 5 Recanati‐Miller Transplantation Institute Mount Sinai Hospital New York New York USA 1 Department of Medicine Translational Transplant Research Center Icahn School of Medicine at Mount Sinai New York New York USA 6 Human Immune Monitoring Core Icahn School of Medicine at Mount Sinai New York New York USA 4 Transplantation Research Center Renal Division Brigham and Women's Hospital Harvard Medical School Boston Massachusetts USA 2 Department of Medicine Division of Nephrology Feinberg School of Medicine Northwestern University Chicago Illinois USA |
| AuthorAffiliation_xml | – name: 1 Department of Medicine Translational Transplant Research Center Icahn School of Medicine at Mount Sinai New York New York USA – name: 3 Renal Unit Department of Medicine University Hospital of Verona Verona Italy – name: 4 Transplantation Research Center Renal Division Brigham and Women's Hospital Harvard Medical School Boston Massachusetts USA – name: 2 Department of Medicine Division of Nephrology Feinberg School of Medicine Northwestern University Chicago Illinois USA – name: 5 Recanati‐Miller Transplantation Institute Mount Sinai Hospital New York New York USA – name: 6 Human Immune Monitoring Core Icahn School of Medicine at Mount Sinai New York New York USA |
| Author_xml | – sequence: 1 givenname: Susan orcidid: 0000-0003-4175-4602 surname: Hartzell fullname: Hartzell, Susan organization: Icahn School of Medicine at Mount Sinai – sequence: 2 givenname: Sofia orcidid: 0000-0001-7120-3866 surname: Bin fullname: Bin, Sofia organization: Icahn School of Medicine at Mount Sinai – sequence: 3 givenname: Claudia orcidid: 0000-0001-9306-1424 surname: Benedetti fullname: Benedetti, Claudia organization: Icahn School of Medicine at Mount Sinai – sequence: 4 givenname: Meredith surname: Haverly fullname: Haverly, Meredith organization: Icahn School of Medicine at Mount Sinai – sequence: 5 givenname: Lorenzo surname: Gallon fullname: Gallon, Lorenzo organization: Northwestern University – sequence: 6 givenname: Gianluigi orcidid: 0000-0002-6004-6196 surname: Zaza fullname: Zaza, Gianluigi organization: University Hospital of Verona – sequence: 7 givenname: Leonardo V. orcidid: 0000-0002-7636-3196 surname: Riella fullname: Riella, Leonardo V. organization: Harvard Medical School – sequence: 8 givenname: Madhav C. orcidid: 0000-0002-9567-4299 surname: Menon fullname: Menon, Madhav C. organization: Icahn School of Medicine at Mount Sinai – sequence: 9 givenname: Sander orcidid: 0000-0002-1635-9136 surname: Florman fullname: Florman, Sander organization: Mount Sinai Hospital – sequence: 10 givenname: Adeeb H. surname: Rahman fullname: Rahman, Adeeb H. organization: Icahn School of Medicine at Mount Sinai – sequence: 11 givenname: John M. surname: Leech fullname: Leech, John M. organization: Icahn School of Medicine at Mount Sinai – sequence: 12 givenname: Peter S. orcidid: 0000-0003-4673-6913 surname: Heeger fullname: Heeger, Peter S. organization: Icahn School of Medicine at Mount Sinai – sequence: 13 givenname: Paolo orcidid: 0000-0001-7837-0923 surname: Cravedi fullname: Cravedi, Paolo email: paolo.cravedi@mssm.edu organization: Icahn School of Medicine at Mount Sinai |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32786152$$D View this record in MEDLINE/PubMed |
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| Keywords | translational research/science immunosuppressant - other immunosuppression/immune modulation kidney transplantation/nephrology immunobiology infection and infectious agents - viral immune regulation |
| Language | English |
| License | 2020 The American Society of Transplantation and the American Society of Transplant Surgeons. This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency. |
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Mar;21(3):911-912 |
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| Snippet | Whether kidney transplant recipients are capable of mounting an effective anti‐severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) adaptive immune... Whether kidney transplant recipients are capable of mounting an effective anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) adaptive immune... |
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| SubjectTerms | Adaptive immunity Anergy Brief Communication Brief Communications CD4 antigen CD8 antigen CD8-Positive T-Lymphocytes - immunology Cell surface Comorbidity Coronaviridae Coronaviruses COVID-19 COVID-19 - epidemiology COVID-19 - immunology Female Flow cytometry Humans immune regulation Immunity, Humoral immunobiology Immunocompromised Host Immunoglobulin G Immunoglobulin M Immunoglobulins Immunological memory immunosuppressant – other Immunosuppression immunosuppression/immune modulation Immunosuppressive agents infection and infectious agents – viral Kidney transplantation Kidney Transplantation - adverse effects kidney transplantation/nephrology Kidney transplants Lymphocytes Lymphocytes B Lymphocytes T Male Memory cells Middle Aged Pandemics Peripheral blood Phenotypes Phenotyping Renal Insufficiency - epidemiology Renal Insufficiency - surgery Retrospective Studies SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 translational research/science Transplant Recipients United States - epidemiology |
| Title | Evidence of potent humoral immune activity in COVID‐19‐infected kidney transplant recipients |
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