KIR <sup>+</sup> CD8 <sup>+</sup> T cells suppress pathogenic T cells and are active in autoimmune diseases and COVID-19-Reference-Cited by-同舟云学术

KIR ⁺ CD8 ⁺ T cells suppress pathogenic T cells and are active in autoimmune diseases and COVID-19

Published:2022-04-15 Issue:6590 Volume:376 Page:
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Li Jing¹^ORCID,Zaslavsky Maxim²^ORCID,Su Yapeng³^ORCID,Guo Jing⁴^ORCID,Sikora Michael J.⁵^ORCID,van Unen Vincent¹^ORCID,Christophersen Asbjørn⁶⁷⁸^ORCID,Chiou Shin-Heng¹^ORCID,Chen Liang¹^ORCID,Li Jiefu⁹,Ji Xuhuai¹⁰^ORCID,Wilhelmy Julie¹^ORCID,McSween Alana M.¹^ORCID,Palanski Brad A.¹¹^ORCID,Mallajosyula Venkata Vamsee Aditya¹^ORCID,Bracey Nathan A.¹^ORCID,Dhondalay Gopal Krishna R.¹²^ORCID,Bhamidipati Kartik¹³,Pai Joy¹³,Kipp Lucas B.¹⁴^ORCID,Dunn Jeffrey E.¹⁴^ORCID,Hauser Stephen L.¹⁵^ORCID,Oksenberg Jorge R.¹⁵,Satpathy Ansuman T.¹⁶^ORCID,Robinson William H.¹⁷¹⁸^ORCID,Dekker Cornelia L.¹⁹^ORCID,Steinmetz Lars M.⁵²⁰²¹^ORCID,Khosla Chaitan¹¹²²²³^ORCID,Utz Paul J.¹¹⁸^ORCID,Sollid Ludvig M.⁶⁷⁸²⁴^ORCID,Chien Yueh-Hsiu¹⁴,Heath James R.³²⁵^ORCID,Fernandez-Becker Nielsen Q.²⁶^ORCID,Nadeau Kari C.¹¹²^ORCID,Saligrama Naresha¹^ORCID,Davis Mark M.¹⁹⁴^ORCID

Affiliation:

1. Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.

2. Program in Computer Science, Stanford University, Stanford, CA, USA.

3. Institute for Systems Biology, Seattle, WA, USA.

4. Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.

5. Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.

6. K.G. Jebsen Coeliac Disease Research Centre, University of Oslo, Oslo, Norway.

7. Institute of Clinical Medicine, University of Oslo, Oslo, Norway.

8. Department of Immunology, University of Oslo, Oslo, Norway.

9. The Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, USA.

10. Human Immune Monitoring Center, Stanford University School of Medicine, Stanford, CA, USA.

11. Department of Chemistry, Stanford University, Stanford, CA, USA.

12. Sean N. Parker Center for Allergy and Asthma Research, Department of Medicine, Stanford University, Stanford, CA, USA.

13. Program in Immunology, Stanford University School of Medicine, Stanford, CA, USA.

14. Division of Neuroimmunology, Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA, USA.

15. Department of Neurology and UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA.

16. Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.

17. VA Palo Alto Health Care System, Palo Alto, CA, USA.

18. Division of Immunology and Rheumatology, Department of Medicine, Stanford University, Stanford, CA, USA.

19. Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.

20. Stanford Genome Technology Center, Stanford University, Palo Alto, CA, USA.

21. European Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg, Germany.

22. Department of Chemical Engineering, Stanford University, Stanford, CA, USA.

23. Stanford ChEM-H, Stanford University, Stanford, CA, USA.

24. Department of Immunology, Oslo University Hospital, Oslo, Norway.

25. Department of Bioengineering, University of Washington, Seattle, WA, USA.

26. Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University, Stanford, CA, USA.

Abstract

In this work, we find that CD8 + T cells expressing inhibitory killer cell immunoglobulin-like receptors (KIRs) are the human equivalent of Ly49 + CD8 + regulatory T cells in mice and are increased in the blood and inflamed tissues of patients with a variety of autoimmune diseases. Moreover, these CD8 + T cells efficiently eliminated pathogenic gliadin-specific CD4 + T cells from the leukocytes of celiac disease patients in vitro. We also find elevated levels of KIR + CD8 + T cells, but not CD4 + regulatory T cells, in COVID-19 patients, correlating with disease severity and vasculitis. Selective ablation of Ly49 + CD8 + T cells in virus-infected mice led to autoimmunity after infection. Our results indicate that in both species, these regulatory CD8 + T cells act specifically to suppress pathogenic T cells in autoimmune and infectious diseases.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

Reference56 articles.

1. New Insights Into the Biology of CD8 Regulatory T Cells

2. Less Mortality but More Relapses in Experimental Allergic Encephalomyelitis in CD8 -/- Mice

3. Role of CD8 + T Cells in Murine Experimental Allergic Encephalomyelitis

4. Inhibition of follicular T-helper cells by CD8+ regulatory T cells is essential for self tolerance

5. CD8+T regulatory cells express the Ly49 Class I MHC receptor and are defective in autoimmune prone B6-Yaa mice

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