Humoral <i>β</i>-cell autoimmunity is rare in patients with the congenital rubella syndrome

Viskari, Hanna; Paronen, Johanna; Keskinen, Päivi; Simell, Satu; Zawilińska, Barbara; Zgórniak-Nowosielska, I; Korhonen, Sari; Ilonen, Jorma; Simell, Olli; Am, Haapala; Knip, Mikael; Hyöty, Heikki

doi:10.1046/j.1365-2249.2003.02244.x

Cited by 29 publications

(12 citation statements)

References 40 publications

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“…As very few cases of CRS have been described in recent years, the immunologic defect underlying this syndrome remains unknown. A T-cell regulatory defect might be implicated, leading to abnormal B-cell function with defective immunoglobulin switch mechanisms, thus facilitating autoimmunity, as in diabetes and thyroiditis, 9,10 and neoplasic disorders. This underlying cellular defect is not corrected with IgG replacement, even in cases with very good control of infectious processes.…”

Section: Discussionmentioning

confidence: 99%

Congenital rubella syndrome, hyper‐IgM syndrome and autoimmunity in an 18‐year‐old girl

Palacín¹,

Castilla²,

Garzón³

et al. 2007

J Paediatrics Child Health

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Congenital rubella syndrome can be associated with disgammaglobulinaemia and autoimmune phenomena in adult and paediatric population. The aim of this article is to present the association between a congenital rubella syndrome with hypogammaglobulinaemia and hyper IgM diagnosed at the age of 8 months and autoimmune manifestations in an 18-year-old girl. A medical chart review of this patient since admission at our institution at 8 months of age was carried out. During infancy she presented the classical manifestations of a rubella syndrome (sensorineural deafness and brain calcifications in basal ganglia) with respiratory and gastrointestinal infections. She was also diagnosed of localised scleroderma and thyroiditis. She has been on intravenous immunoglobulin since diagnosis, with rapid normalisation of IgG and IgM levels, decreased incidence of infectious processes, but with persistent autoimmune phenomena. At 18 years of age she was admitted because of a thyroid mass. Fine needle aspiration biopsy was not conclusive and thyroidectomy was performed. Pathology studies showed no malignancy. She is now on replacement therapy with thyroid hormones. Our aim is to emphasise the importance of the association between autoimmune phenomena in patients with immunodeficiencies, even secondary to some infections, and the increased frequency of malignancies owing to the persistent immunologic defect in this syndrome.

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Section: Discussionmentioning

confidence: 99%

Congenital rubella syndrome, hyper‐IgM syndrome and autoimmunity in an 18‐year‐old girl

Palacín¹,

Castilla²,

Garzón³

et al. 2007

J Paediatrics Child Health

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“…The methods used to diagnose diabetes were heterogeneous, and clinical characteristics were poorly described, impeding the interpretation of the results. A study of 25 Finnish and 12 Polish patients reported no signs of beta‐cell autoimmunity in participants with congenital rubella syndrome (CRS) …”

Section: Resultsmentioning

confidence: 99%

Maternal virus infections in pregnancy and type 1 diabetes in their offspring: Systematic review and meta‐analysis of observational studies

Allen

Kim

Rawlinson

et al. 2018

Reviews in Medical Virology

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Virus infections are implicated in the development of type 1 diabetes based on epidemiological, clinical, in vitro cell-based and molecular studies, and animal models. We reviewed the association between virus infections in pregnant women and development of islet autoimmunity or type 1 diabetes in their offspring. We performed a systematic review and meta-analysis, analysed using random effects models, of human studies from Medline and EMBASE without language restriction. Inclusion criteria were as follows: cohort and case-control studies measuring viral nucleic acid in blood, stool, urine, or tissue, or serological tests for viruses, in pregnant women whose offspring developed islet autoimmunity and/or type 1 diabetes. All studies required sufficient data to calculate odds ratios and 95% confidence intervals. The 10 studies (4 case control, 6 nested-case control) that met the eligibility criteria included 2992 participants (953 offspring, 2039 mothers), with varying study design. The 2 outcomes examined were islet autoimmunity (n = 466) and type 1 diabetes (n = 2526). Meta-analysis showed a significant association between virus infection during pregnancy and clinical type 1 diabetes during childhood (odds ratio 2·16, 95% CI 1·22-3·80; P = 0·008; heterogeneity X = 1·65, I = 40%), but no association with islet autoimmunity (1·45, 0·63-3·31; P = 0·38; X = 1·34, I = 25%). The increased risk of type 1 diabetes following maternal virus infection is consistent with viraemia involving the fetus during pregnancy and suggests a potential causative link between antenatal infection and type 1 diabetes. Larger prospective birth studies with more frequent sampling, and pathogenesis studies, are required to more clearly establish an aetiological link.

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“…It has been shown that the percentage of subjects with antibodies against islet cells is increased in patients with congenital rubella syndrome compared with noninfected subjects 46. However, a more recent study by Viskari et al was not able to demonstrate such a correlation between congenital rubella syndrome and the development of autoantibodies against islet antigens 116. These data led the authors to conclude that diabetes development in subjects with congenital rubella syndrome may not be immune‐mediated.…”

Section: Viruses In T1dmentioning

confidence: 96%

Viral infections as potential triggers of type 1 diabetes

Werf

Kroese

Rozing

et al. 2007

Diabetes Metabolism Res

192

136

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SummaryDuring the last decades, the incidence of type 1 diabetes (T1D) has increased significantly, reaching percentages of 3% annually worldwide. This increase suggests that besides genetical factors environmental perturbations (including viral infections) are also involved in the pathogenesis of T1D. T1D has been associated with viral infections including enteroviruses, rubella, mumps, rotavirus, parvovirus and cytomegalovirus (CMV). Although correlations between clinical presentation with T1D and the occurrence of a viral infection that precedes the development of overt disease have been recognized, causalities between viruses and the diabetogenic process are still elusive and difficult to prove in humans. The use of experimental animal models is therefore indispensable, and indeed more insight in the mechanism by which viruses can modulate diabetogenesis has been provided by studies in rodent models for T1D such as the biobreeding (BB) rat, nonobese diabetic (NOD) mouse or specific transgenic mouse strains. Data from experimental animals as well as in vitro studies indicate that various viruses are clearly able to modulate the development of T1D via different mechanisms, including direct β-cell lysis, bystander activation of autoreactive T cells, loss of regulatory T cells and molecular mimicry. Data obtained in rodents and in vitro systems have improved our insight in the possible role of viral infections in the pathogenesis of human T1D. Future studies will hopefully reveal which human viruses are causally involved in the induction of T1D and this knowledge may provide directions on how to deal with viral infections in diabetes-susceptible individuals in order to delay or even prevent the diabetogenic process.

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Humoral β-cell autoimmunity is rare in patients with the congenital rubella syndrome

Cited by 29 publications

References 40 publications

Congenital rubella syndrome, hyper‐IgM syndrome and autoimmunity in an 18‐year‐old girl

Congenital rubella syndrome, hyper‐IgM syndrome and autoimmunity in an 18‐year‐old girl

Maternal virus infections in pregnancy and type 1 diabetes in their offspring: Systematic review and meta‐analysis of observational studies

Viral infections as potential triggers of type 1 diabetes

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