Chronic inflammation and extracellular matrix-specific autoimmunity following inadvertent periarticular influenza vaccination.


Journal

Journal of autoimmunity
ISSN: 1095-9157
Titre abrégé: J Autoimmun
Pays: England
ID NLM: 8812164

Informations de publication

Date de publication:
11 2021
Historique:
received: 18 05 2021
revised: 27 07 2021
accepted: 05 08 2021
pubmed: 18 8 2021
medline: 11 3 2022
entrez: 17 8 2021
Statut: ppublish

Résumé

Viral infections may trigger autoimmunity in genetically predisposed individuals. Immunizations mimic viral infections immunologically, but only in rare instances vaccinations coincide with the onset of autoimmunity. Inadvertent vaccine injection into periarticular shoulder tissue can cause inflammatory tissue damage ('shoulder injury related to vaccine administration, SIRVA). Thus, this accident provides a model to study if vaccine-induced pathogen-specific immunity accompanied by a robust inflammatory insult may trigger autoimmunity in specific genetic backgrounds. We studied 16 otherwise healthy adults with suspected SIRVA occurring following a single work-related influenza immunization campaign in 2017. We performed ultrasound, immunophenotypic analyses, HLA typing, and influenza- and self-reactivity functional immunoassays. Vaccine-related bone toxicity and T cell/osteoclast interactions were assessed in vitro. Twelve of the 16 subjects had evidence of inflammatory tissue damage on imaging, including bone erosions in six. Tissue damage was associated with a robust peripheral blood T and B cell activation signature and extracellular matrix-reactive autoantibodies. All subjects with erosions were HLA-DRB1*04 positive and showed extracellular matrix-reactive HLA-DRB1*04 restricted T cell responses targeting heparan sulfate proteoglycan (HSPG). Antigen-specific T cells potently activated osteoclasts via RANK/RANK-L, and the osteoclast activation marker Trap5b was high in sera of patients with an erosive shoulder injury. In vitro, the vaccine component alpha-tocopheryl succinate recapitulated bone toxicity and stimulated osteoclasts. Auto-reactivity was transient, with no evidence of progression to rheumatoid arthritis or overt autoimmune disease. Vaccine misapplication, potentially a genetic predisposition, and vaccine components contribute to SIRVA. The association with autoimmunity risk allele HLA-DRB1*04 needs to be further investigated. Despite transient autoimmunity, SIRVA was not associated with progression to autoimmune disease during two years of follow-up.

Sections du résumé

BACKGROUND
Viral infections may trigger autoimmunity in genetically predisposed individuals. Immunizations mimic viral infections immunologically, but only in rare instances vaccinations coincide with the onset of autoimmunity. Inadvertent vaccine injection into periarticular shoulder tissue can cause inflammatory tissue damage ('shoulder injury related to vaccine administration, SIRVA). Thus, this accident provides a model to study if vaccine-induced pathogen-specific immunity accompanied by a robust inflammatory insult may trigger autoimmunity in specific genetic backgrounds.
METHODS
We studied 16 otherwise healthy adults with suspected SIRVA occurring following a single work-related influenza immunization campaign in 2017. We performed ultrasound, immunophenotypic analyses, HLA typing, and influenza- and self-reactivity functional immunoassays. Vaccine-related bone toxicity and T cell/osteoclast interactions were assessed in vitro.
FINDINGS
Twelve of the 16 subjects had evidence of inflammatory tissue damage on imaging, including bone erosions in six. Tissue damage was associated with a robust peripheral blood T and B cell activation signature and extracellular matrix-reactive autoantibodies. All subjects with erosions were HLA-DRB1*04 positive and showed extracellular matrix-reactive HLA-DRB1*04 restricted T cell responses targeting heparan sulfate proteoglycan (HSPG). Antigen-specific T cells potently activated osteoclasts via RANK/RANK-L, and the osteoclast activation marker Trap5b was high in sera of patients with an erosive shoulder injury. In vitro, the vaccine component alpha-tocopheryl succinate recapitulated bone toxicity and stimulated osteoclasts. Auto-reactivity was transient, with no evidence of progression to rheumatoid arthritis or overt autoimmune disease.
CONCLUSION
Vaccine misapplication, potentially a genetic predisposition, and vaccine components contribute to SIRVA. The association with autoimmunity risk allele HLA-DRB1*04 needs to be further investigated. Despite transient autoimmunity, SIRVA was not associated with progression to autoimmune disease during two years of follow-up.

Identifiants

pubmed: 34403915
pii: S0896-8411(21)00122-0
doi: 10.1016/j.jaut.2021.102714
pii:
doi:

Substances chimiques

HLA-DRB1 Chains 0
HLA-DRB1*04 antigen 0
Heparan Sulfate Proteoglycans 0
Influenza Vaccines 0
Receptor Activator of Nuclear Factor-kappa B 0
ACP5 protein, human EC 3.1.3.2
Tartrate-Resistant Acid Phosphatase EC 3.1.3.2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

102714

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Auteurs

Julia R Hirsiger (JR)

Translational Immunology, Department of Biomedicine, University of Basel, Basel, Switzerland.

Giorgio Tamborrini (G)

Ultrasound Center for Rheumatology (UZR), Basel, Switzerland; Rheumatology Clinic, University Hospital Basel, Basel, Switzerland.

Dorothee Harder (D)

Department of Radiology, University Hospital Basel, Basel, Switzerland.

Glenn R Bantug (GR)

Immunobiology Lab, Department Biomedicine, University of Basel, Basel, Switzerland.

Gideon Hoenger (G)

HLA-Diagnostics and Immunogenetics, Department of Laboratory Medicine, University Hospital Basel, Basel, Switzerland.

Mike Recher (M)

Immunodeficiency Lab, Department Biomedicine, University of Basel, Basel, Switzerland.

Christian Marx (C)

Rheumatology Zürcher Oberland (RZO), Uster, Switzerland.

Quan-Zhen Li (QZ)

Department of Immunology & Internal Medicine, IIMT Microarray Core Facility, University of Texas Southwestern Medical Center, USA.

Ivan Martin (I)

Laboratory of Tissue Engineering, Departments of Surgery and Biomedicine, University Hospital of Basel, University of Basel, Basel, Switzerland.

Christoph Hess (C)

Immunobiology Lab, Department Biomedicine, University of Basel, Basel, Switzerland.

Arnaud Scherberich (A)

Laboratory of Tissue Engineering, Departments of Surgery and Biomedicine, University Hospital of Basel, University of Basel, Basel, Switzerland.

Thomas Daikeler (T)

Rheumatology Clinic, University Hospital Basel, Basel, Switzerland.

Christoph T Berger (CT)

Translational Immunology, Department of Biomedicine, University of Basel, Basel, Switzerland; Interdisciplinary Center for Immunology, Departments of Dermatology, Internal Medicine, and Rheumatology, University Hospital Basel, Basel, Switzerland. Electronic address: christoph.berger@usb.ch.

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Classifications MeSH