Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer
Summary: Infection, autoimmunity, and cancer are principal human health challenges of the 21st century. Often regarded as distinct ends of the immunological spectrum, recent studies hint at potential overlap between these diseases. For example, inflammation can be pathogenic in infection and autoimm...
| Main Authors: | , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2024-03-01
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| Series: | Cell Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124724002006 |
| _version_ | 1797287635200245760 |
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| author | Daniel G. Chen Jingyi Xie Jongchan Choi Rachel H. Ng Rongyu Zhang Sarah Li Rick Edmark Hong Zheng Ben Solomon Katie M. Campbell Egmidio Medina Antoni Ribas Purvesh Khatri Lewis L. Lanier Philip J. Mease Jason D. Goldman Yapeng Su James R. Heath |
| author_facet | Daniel G. Chen Jingyi Xie Jongchan Choi Rachel H. Ng Rongyu Zhang Sarah Li Rick Edmark Hong Zheng Ben Solomon Katie M. Campbell Egmidio Medina Antoni Ribas Purvesh Khatri Lewis L. Lanier Philip J. Mease Jason D. Goldman Yapeng Su James R. Heath |
| author_sort | Daniel G. Chen |
| collection | DOAJ |
| description | Summary: Infection, autoimmunity, and cancer are principal human health challenges of the 21st century. Often regarded as distinct ends of the immunological spectrum, recent studies hint at potential overlap between these diseases. For example, inflammation can be pathogenic in infection and autoimmunity. T resident memory (TRM) cells can be beneficial in infection and cancer. However, these findings are limited by size and scope; exact immunological factors shared across diseases remain elusive. Here, we integrate large-scale deeply clinically and biologically phenotyped human cohorts of 526 patients with infection, 162 with lupus, and 11,180 with cancer. We identify an NKG2A+ immune bias as associative with protection against disease severity, mortality, and autoimmune/post-acute chronic disease. We reveal that NKG2A+ CD8+ T cells correlate with reduced inflammation and increased humoral immunity and that they resemble TRM cells. Our results suggest NKG2A+ biases as a cross-disease factor of protection, supporting suggestions of immunological overlap between infection, autoimmunity, and cancer. |
| first_indexed | 2024-03-07T18:36:12Z |
| format | Article |
| id | doaj.art-66da9e46dc354e898aea61faa116e5ae |
| institution | Directory Open Access Journal |
| issn | 2211-1247 |
| language | English |
| last_indexed | 2024-03-07T18:36:12Z |
| publishDate | 2024-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cell Reports |
| spelling | doaj.art-66da9e46dc354e898aea61faa116e5ae2024-03-02T04:53:59ZengElsevierCell Reports2211-12472024-03-01433113872Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancerDaniel G. Chen0Jingyi Xie1Jongchan Choi2Rachel H. Ng3Rongyu Zhang4Sarah Li5Rick Edmark6Hong Zheng7Ben Solomon8Katie M. Campbell9Egmidio Medina10Antoni Ribas11Purvesh Khatri12Lewis L. Lanier13Philip J. Mease14Jason D. Goldman15Yapeng Su16James R. Heath17Institute of Systems Biology, Seattle, WA, USA; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA; Clinical Research Division, Program in Immunology, Fred Hutchinson Cancer Research Center, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USA; Molecular Engineering & Sciences Institute, University of Washington, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USA; Department of Bioengineering, University of Washington, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USA; Department of Bioengineering, University of Washington, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USAInstitute for Immunity, Transplantation and Infection, School of Medicine, Stanford University, Stanford, CA, USA; Center for Biomedical Informatics Research, Department of Medicine, School of Medicine, Stanford University, Stanford, CA, USADepartment of Pediatrics, Division of Allergy and Immunology, Stanford School of Medicine, Stanford, CA, USADepartment of Medicine, Division of Hematology–Oncology, University of California, Los Angeles, Los Angeles, CA, USA; Parker Institute for Cancer Immunotherapy, San Francisco, CA, USADepartment of Medicine, Division of Hematology–Oncology, University of California, Los Angeles, Los Angeles, CA, USADepartment of Medicine, Division of Hematology–Oncology, University of California, Los Angeles, Los Angeles, CA, USA; Jonsson Comprehensive Cancer Center at the University of California, Los Angeles, CA, USA; Parker Institute for Cancer Immunotherapy, San Francisco, CA, USAInstitute for Immunity, Transplantation and Infection, School of Medicine, Stanford University, Stanford, CA, USA; Center for Biomedical Informatics Research, Department of Medicine, School of Medicine, Stanford University, Stanford, CA, USADepartment of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA, USA; Parker Institute for Cancer Immunotherapy, San Francisco, CA, USASwedish Center for Research and Innovation, Swedish Medical Center, Seattle, WA, USA; Providence St. Joseph Health, Renton, WA, USASwedish Center for Research and Innovation, Swedish Medical Center, Seattle, WA, USA; Providence St. Joseph Health, Renton, WA, USA; Division of Allergy and Infectious Diseases, University of Washington, Seattle, WA, USAVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA; Clinical Research Division, Program in Immunology, Fred Hutchinson Cancer Research Center, Seattle, WA, USAInstitute of Systems Biology, Seattle, WA, USA; Department of Bioengineering, University of Washington, Seattle, WA, USA; Parker Institute for Cancer Immunotherapy, San Francisco, CA, USA; Corresponding authorSummary: Infection, autoimmunity, and cancer are principal human health challenges of the 21st century. Often regarded as distinct ends of the immunological spectrum, recent studies hint at potential overlap between these diseases. For example, inflammation can be pathogenic in infection and autoimmunity. T resident memory (TRM) cells can be beneficial in infection and cancer. However, these findings are limited by size and scope; exact immunological factors shared across diseases remain elusive. Here, we integrate large-scale deeply clinically and biologically phenotyped human cohorts of 526 patients with infection, 162 with lupus, and 11,180 with cancer. We identify an NKG2A+ immune bias as associative with protection against disease severity, mortality, and autoimmune/post-acute chronic disease. We reveal that NKG2A+ CD8+ T cells correlate with reduced inflammation and increased humoral immunity and that they resemble TRM cells. Our results suggest NKG2A+ biases as a cross-disease factor of protection, supporting suggestions of immunological overlap between infection, autoimmunity, and cancer.http://www.sciencedirect.com/science/article/pii/S2211124724002006CP: Immunology |
| spellingShingle | Daniel G. Chen Jingyi Xie Jongchan Choi Rachel H. Ng Rongyu Zhang Sarah Li Rick Edmark Hong Zheng Ben Solomon Katie M. Campbell Egmidio Medina Antoni Ribas Purvesh Khatri Lewis L. Lanier Philip J. Mease Jason D. Goldman Yapeng Su James R. Heath Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer Cell Reports CP: Immunology |
| title | Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer |
| title_full | Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer |
| title_fullStr | Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer |
| title_full_unstemmed | Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer |
| title_short | Integrative systems biology reveals NKG2A-biased immune responses correlate with protection in infectious disease, autoimmune disease, and cancer |
| title_sort | integrative systems biology reveals nkg2a biased immune responses correlate with protection in infectious disease autoimmune disease and cancer |
| topic | CP: Immunology |
| url | http://www.sciencedirect.com/science/article/pii/S2211124724002006 |
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