HLA‐DQ‐conferred risk for type 1 diabetes does not alter neutralizing antibody response to a widely used enterovirus vaccine, the poliovirus vaccine

Author:

Sioofy‐Khojine Amir‐Babak1ORCID,Lehtonen Jussi P.1,Nurminen Noora1,Laiho Jutta E.1,Toppari Jorma23,Veijola Riitta45,Lempainen Johanna267,Ilonen Jorma6,Knip Mikael8910,Hyöty Heikki111

Affiliation:

1. Department of Virology, Faculty of Medicine and Health Technology Tampere University Tampere Finland

2. Department of Paediatrics Turku University Hospital Turku Finland

3. Faculty of Medicine, Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology University of Turku Turku Finland

4. Department for Children and Adolescents Oulu University Hospital Oulu Finland

5. Department of Paediatrics, MRC Oulu University of Oulu Oulu Finland

6. Immunogenetics Laboratory, Institute of Biomedicine University of Turku Turku Finland

7. Department of Clinical Microbiology Turku University Hospital Turku Finland

8. Research Program for Clinical and Molecular Metabolism, Faculty of Medicine University of Helsinki Helsinki Finland

9. Pediatric Research Centre, New Children's Hospital Helsinki University Hospital Helsinki Finland

10. Tampere Centre for Child Health Research Tampere University Hospital Tampere Finland

11. Fimlab Laboratories Pirkanmaa Hospital District Tampere Finland

Abstract

AbstractThis study investigated whether children with HLA‐DQ‐conferred risk for type 1 diabetes (T1D) have an altered immune response to the widely‐used enterovirus vaccine, namely poliovirus vaccine, and whether initiation of autoimmunity to pancreatic islets modulates this response. Neutralizing antibodies induced by the inactivated poliovirus vaccine against poliovirus type 1 (Salk) were analysed as a marker of protective immunity at the age of 18 months in a prospective birth cohort. No differences were observed in antibody titers between children with and without genetic risk for T1D (odds ratio [OR] = 0.90 [0.83, 1.06], p = 0.30). In the presence of the genetic risk, no difference was observed between children with and without islet autoimmunity (OR = 1.00 [0.78, 1.28], p = 1.00). This did not change when only children with the autoimmunity before 18 months of age were included in the analyses (OR = 1.00 [0.85, 1.18], p = 1.00). No effect was observed when groups were stratified based on autoantigen specificity of the first‐appearing autoantibody (IAA or GADA). The children in each comparison group were matched for sex, calendar year and month of birth, and municipality. Accordingly, we found no indication that children who are at risk to develop islet autoimmunity would have a compromised humoral immune response which could have increased their susceptibility for enterovirus infections. In addition, the proper immune response supports the idea of testing novel enterovirus vaccines for the prevention of T1D among these individuals.

Publisher

Wiley

Subject

Infectious Diseases,Virology

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