The impact of hybrid immunity on immune responses after SARS-CoV-2 vaccination in persons with multiple sclerosis treated with disease-modifying therapies.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
12 2023
Historique:
revised: 22 06 2023
received: 09 11 2022
accepted: 27 07 2023
medline: 10 11 2023
pubmed: 31 7 2023
entrez: 31 7 2023
Statut: ppublish

Résumé

Hybrid immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develops from a combination of natural infection and vaccine-generated immunity. Multiple sclerosis (MS) disease-modifying therapies (DMTs) have the potential to impact humoral and cellular immunity induced by SARS-CoV-2 vaccination and infection. The aims were to compare antibody and T-cell responses after SARS-CoV-2 mRNA vaccination in persons with MS (pwMS) treated with different DMTs and to assess differences between naïvely vaccinated pwMS and pwMS with hybrid immunity vaccinated following a previous SARS-CoV-2 infection. Antibody and T-cell responses were determined in pwMS at baseline and 4 and 12 weeks after the second dose of SARS-CoV-2 vaccination in 143 pwMS with or without previous SARS-CoV-2 infection and 40 healthy controls (HCs). The MS cohort comprised natalizumab (n = 22), dimethylfumarate (n = 23), fingolimod (n = 38), cladribine (n = 30), alemtuzumab (n = 17) and teriflunomide (n = 13) treated pwMS. Immunoglobulin G antibody responses to SARS-CoV-2 antigens were measured using a multiplex bead assay and FluoroSpot was used to assess T-cell responses (interferon γ and interleukin 13). Humoral and T-cell responses to vaccination were comparable between naïvely vaccinated HCs and pwMS treated with natalizumab, dimethylfumarate, cladribine, alemtuzumab and teriflunomide, but were suppressed in fingolimod-treated pwMS. Both fingolimod-treated pwMS and HCs vaccinated following a previous SARS-CoV-2 infection had higher antibody levels 4 weeks after vaccination compared to naïvely vaccinated individuals. Antibody and interferon γ levels 12 weeks after vaccination were positively correlated with time from last treatment course of cladribine. These findings are of relevance for infection risk mitigation and for vaccination strategies amongst pwMS undergoing DMT.

Sections du résumé

BACKGROUND AND PURPOSE
Hybrid immunity to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) develops from a combination of natural infection and vaccine-generated immunity. Multiple sclerosis (MS) disease-modifying therapies (DMTs) have the potential to impact humoral and cellular immunity induced by SARS-CoV-2 vaccination and infection. The aims were to compare antibody and T-cell responses after SARS-CoV-2 mRNA vaccination in persons with MS (pwMS) treated with different DMTs and to assess differences between naïvely vaccinated pwMS and pwMS with hybrid immunity vaccinated following a previous SARS-CoV-2 infection.
METHODS
Antibody and T-cell responses were determined in pwMS at baseline and 4 and 12 weeks after the second dose of SARS-CoV-2 vaccination in 143 pwMS with or without previous SARS-CoV-2 infection and 40 healthy controls (HCs). The MS cohort comprised natalizumab (n = 22), dimethylfumarate (n = 23), fingolimod (n = 38), cladribine (n = 30), alemtuzumab (n = 17) and teriflunomide (n = 13) treated pwMS. Immunoglobulin G antibody responses to SARS-CoV-2 antigens were measured using a multiplex bead assay and FluoroSpot was used to assess T-cell responses (interferon γ and interleukin 13).
RESULTS
Humoral and T-cell responses to vaccination were comparable between naïvely vaccinated HCs and pwMS treated with natalizumab, dimethylfumarate, cladribine, alemtuzumab and teriflunomide, but were suppressed in fingolimod-treated pwMS. Both fingolimod-treated pwMS and HCs vaccinated following a previous SARS-CoV-2 infection had higher antibody levels 4 weeks after vaccination compared to naïvely vaccinated individuals. Antibody and interferon γ levels 12 weeks after vaccination were positively correlated with time from last treatment course of cladribine.
CONCLUSION
These findings are of relevance for infection risk mitigation and for vaccination strategies amongst pwMS undergoing DMT.

Identifiants

pubmed: 37522464
doi: 10.1111/ene.16015
doi:

Substances chimiques

teriflunomide 1C058IKG3B
Cladribine 47M74X9YT5
Natalizumab 0
COVID-19 Vaccines 0
Interferon-gamma 82115-62-6
Alemtuzumab 3A189DH42V
Dimethyl Fumarate FO2303MNI2
Fingolimod Hydrochloride G926EC510T
Antibodies 0
Antibodies, Viral 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3789-3798

Informations de copyright

© 2023 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.

Références

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Auteurs

Monika Rabenstein (M)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.
Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.
Department of Neurology, Faculty of Medicine and University Hospital, University of Cologne, Cologne, Germany.

Olivia G Thomas (OG)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.
Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.

Giorgia Carlin (G)

Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.

Mohsen Khademi (M)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.

Klara Asplund Högelin (KA)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.

Clas Malmeström (C)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Markus Axelsson (M)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Anne Frandsen Brandt (AF)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Guro Gafvelin (G)

Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.

Hans Grönlund (H)

Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.

Ingrid Kockum (I)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.

Fredrik Piehl (F)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.

Jan Lycke (J)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Tomas Olsson (T)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.

Tara Hessa (T)

Therapeutic Immune Design, Department of Clinical Neuroscience, Center for Molecular Medicine L8:02, Karolinska Institute, Stockholm, Sweden.
Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine L8:04, Karolinska Institute, Stockholm, Sweden.

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