Coxsackievirus infection induces direct pancreatic β cell killing but poor antiviral CD8 <sup>+</sup> T cell responses-Reference-Cited by-同舟云学术

Coxsackievirus infection induces direct pancreatic β cell killing but poor antiviral CD8 ⁺ T cell responses

Published:2024-03-08 Issue:10 Volume:10 Page:
ISSN:2375-2548
Container-title:Science Advances
language:en
Short-container-title:Sci. Adv.

Author:

Vecchio Federica¹^ORCID,Carré Alexia¹^ORCID,Korenkov Daniil¹^ORCID,Zhou Zhicheng¹^ORCID,Apaolaza Paola²³^ORCID,Tuomela Soile⁴,Burgos-Morales Orlando¹,Snowhite Isaac⁵⁶^ORCID,Perez-Hernandez Javier¹^ORCID,Brandao Barbara¹^ORCID,Afonso Georgia¹^ORCID,Halliez Clémentine¹⁷^ORCID,Kaddis John⁶⁸^ORCID,Kent Sally C.⁹,Nakayama Maki¹⁰^ORCID,Richardson Sarah J.¹¹^ORCID,Vinh Joelle¹²^ORCID,Verdier Yann¹²^ORCID,Laiho Jutta¹³^ORCID,Scharfmann Raphael¹,Solimena Michele³¹⁴,Marinicova Zuzana³¹⁴^ORCID,Bismuth Elise¹⁵,Lucidarme Nadine¹⁶,Sanchez Janine¹⁷^ORCID,Bustamante Carmen¹⁷,Gomez Patricia¹⁷^ORCID,Buus Soren¹⁸^ORCID, ,You Sylvaine¹¹⁹^ORCID,Pugliese Alberto⁵⁶^ORCID,Hyoty Heikki¹³²⁰²¹^ORCID,Rodriguez-Calvo Teresa²³^ORCID,Flodstrom-Tullberg Malin⁴^ORCID,Mallone Roberto¹⁷¹⁹^ORCID

Affiliation:

1. Université Paris Cité, Institut Cochin, CNRS, INSERM, Paris, France.

2. Institute of Diabetes Research, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich-Neuherberg, Germany.

3. German Center for Diabetes Research (DZD e.V.), Neuherberg, Germany.

4. Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.

5. Diabetes Research Institute, Leonard Miller School of Medicine, University of Miami, Miami, FL, USA.

6. Department of Diabetes Immunology, Arthur Riggs Diabetes and Metabolism Research Institute, Beckman Research Institute, City of Hope, Duarte, CA, USA.

7. Assistance Publique Hôpitaux de Paris, Service de Diabétologie et Immunologie Clinique, Cochin Hospital, Paris, France.

8. Department of Diabetes and Cancer Discovery Science, Arthur Riggs Diabetes and Metabolism Research Institute, Beckman Research Institute, City of Hope, Duarte, CA, USA.

9. Diabetes Center of Excellence, Department of Medicine, University of Massachusetts Medical Chan School, Worcester, MA, USA.

10. Barbara Davis Center for Diabetes, University of Colorado School of Medicine, Aurora, CO, USA.

11. Islet Biology Exeter (IBEx), Exeter Centre of Excellence for Diabetes Research (EXCEED), Department of Clinical and Biomedical Sciences, University of Exeter Medical School, Exeter, UK.

12. ESPCI Paris, PSL University, Spectrométrie de Masse Biologique et Protéomique, CNRS UMR8249, Paris, France.

13. Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.

14. Paul Langerhans Institute Dresden (PLID), Helmholtz Munich, University Hospital and Faculty of Medicine, TU Dresden, Dresden, Germany.

15. Assistance Publique Hôpitaux de Paris, Service d’Endocrinologie Pédiatrique, Robert Debré Hospital, Paris, France.

16. Assistance Publique Hôpitaux de Paris, Service de Pédiatrie, Jean Verdier Hospital, Bondy, France.

17. Department of Pediatrics, Division of Pediatric Endocrinology, Leonard Miller School of Medicine, University of Miami, Miami, FL, USA.

18. Department of Immunology and Microbiology, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.

19. Indiana Biosciences Research Institute, Indianapolis, IN, USA.

20. Fimlab Laboratories, Tampere, Finland.

21. Department of Pediatrics, Tampere University Hospital, Tampere, Finland.

Abstract

Coxsackievirus B (CVB) infection of pancreatic β cells is associated with β cell autoimmunity and type 1 diabetes. We investigated how CVB affects human β cells and anti-CVB T cell responses. β cells were efficiently infected by CVB in vitro, down-regulated human leukocyte antigen (HLA) class I, and presented few, selected HLA-bound viral peptides. Circulating CD8 + T cells from CVB–seropositive individuals recognized a fraction of these peptides; only another subfraction was targeted by effector/memory T cells that expressed exhaustion marker PD-1. T cells recognizing a CVB epitope cross-reacted with β cell antigen GAD. Infected β cells, which formed filopodia to propagate infection, were more efficiently killed by CVB than by CVB-reactive T cells. Our in vitro and ex vivo data highlight limited CD8 + T cell responses to CVB, supporting the rationale for CVB vaccination trials for type 1 diabetes prevention. CD8 + T cells recognizing structural and nonstructural CVB epitopes provide biomarkers to differentially follow response to infection and vaccination.

Publisher

American Association for the Advancement of Science (AAAS)

Link

https://www.science.org/doi/pdf/10.1126/sciadv.adl1122

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