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Decreased In Vitro Type 1 Immune Response Against Coxsackie Virus B4 in Children With Type 1 Diabetes

¹ Division of Pediatrics and Diabetes Research Centre, Department of Molecular and Clinical Medicine, Linköping University, Linköping, Sweden
² Laboratory for Immunobiology, Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland
³ Enterovirus Laboratory, Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland
⁴ Turku Immunology Centre and Department of Virology, University of Turku, Turku, Finland

Address correspondence and reprint requests to Dr. Susanne Skarsvik, Clinical and Experimental Research, Faculty of Health Sciences, Linköping University, S-581 85 Linköping, Sweden. E-mail: susanne.skarsvik{at}imk.liu.se

Enteroviruses, particularly Coxsackie virus B4 (CVB4), are considered to be involved in the pathogenesis of type 1 diabetes. We wanted to compare the characteristics of T-cell immune response to CVB4 in children with type 1 diabetes and healthy children with and without HLA risk-associated haplotypes (HLA-DR3-DQ2 or HLA-DR4-DQ8) for type 1 diabetes. Peripheral blood mononuclear cells (PBMCs) were isolated and cultured with CVB4 and analyzed for cytokine and chemokine receptors by flow cytometry and for expression of transcription factors Tbet and GATA-3 by RT-PCR and Western blot. Culture supernatants were analyzed for secretion of -interferon (IFN-). In children with type 1 diabetes, a decreased percentage of T-cells expressed CCR2, CXCR6, interleukin (IL)-18R, and IL-12Rß₂-chain after in vitro stimulation with CVB4 in comparison with healthy children with or without HLA risk genotype. Moreover, we found that children with type 1 diabetes had decreased IFN- secretion and expression of Tbet, both on mRNA and protein level, in CVB4-stimulated PBMCs. Accordingly, children with type 1 diabetes show an impaired type 1 immune response against CVB4 compared with healthy children. This may lead to a delayed clearance of the virus and, at least partly, explain why children with type 1 diabetes may be more prone to CVB4 infections and related complications, such as ß-cell damage.

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