Islet autoantibodies in cord blood: maternal, fetal, or neither?

Rewers, Marian

doi:10.1002/dmrr.240

Cited by 6 publications

(5 citation statements)

References 43 publications

(19 reference statements)

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“…Other studies have reported frequencies of around 3%. 44 There was a lower number of high binders in 2001 (0.3%) as compared to the other years (0.6%) due to a downward drift in the GAD65Ab assay during the middle of 2001. However, this underestimation in 2001 likely reduced the significance of our results as a repeat of the analysis with the 2001 newborns omitted showed a stronger consistent seasonal quarterly trend in newborns with high GAD65Ab binding.…”

Section: Discussionmentioning

confidence: 90%

Cord blood islet autoantibodies and seasonal association with the type 1 diabetes high-risk genotype

et al. 2008

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Objective: Human leukocyte antigen DQ (HLA-DQ) genetic factors and islet autoantibodies are strongly associated with type 1 diabetes (T1D) and are currently used to predict T1D. This study examined whether islet autoantibodies in the cord blood of newborns to nondiabetic mothers were associated with the (T1D) high-risk genotype HLA-DQ2/8, gestational infections or both.Study Design: Cord blood samples were taken from 33 683 newborns and used for HLA typing and analyses of islet autoantibodies. Parents completed questionnaires when the child was 2 months of age.

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Section: Discussionmentioning

confidence: 90%

Cord blood islet autoantibodies and seasonal association with the type 1 diabetes high-risk genotype

et al. 2008

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“…TEDDY was designed to obtain blood samples from 3–4 months of age and onwards every three months to detect a first appearing β-cell autoantibody. Since mothers may be β-cell autoantibody positive, whether with T1D (36, 37), or not (25, 37–39), we excluded FDR mothers and adjusted for maternal β-cell autoantibody exposure that was determined by analysing IAA, GADA and IA-2A in a blood sample from the mothers when the child was 6–9 months old (1). In our analysis, 51 children were found to be exposed to maternal autoantibodies but there was no association with risk of IAA or GADA in the child.…”

Section: Discussionmentioning

confidence: 99%

Gestational respiratory infections interacting with offspring HLA and CTLA-4 modifies incident β-cell autoantibodies

Lynch¹,

Lee²,

Törn³

et al. 2018

Journal of Autoimmunity

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β-cell autoantibodies against insulin (IAA), GAD65 (GADA) and IA-2 (IA-2A) precede onset of childhood type 1 diabetes (T1D). Incidence of the first appearing β-cell autoantibodies peaks at a young age and is patterned by T1D-associated genes, suggesting an early environmental influence. Here, we tested if gestational infections and interactions with child's human leukocyte antigen (HLA) and non-HLA genes affected the appearance of the first β-cell autoantibody. Singletons of mothers without diabetes (n = 7472) with T1D-associated HLA-DR-DQ genotypes were prospectively followed quarterly through the first 4 years of life, then semiannually until age 6 years, using standardized autoantibody analyses. Maternal infections during pregnancy were assessed via questionnaire 3-4.5 months post-delivery. Polymorphisms in twelve non-HLA genes associated with the first appearing β-cell autoantibodies were included in a Cox regression analysis. IAA predominated as the first appearing β-cell autoantibody in younger children (n = 226, median age at seroconversion 1.8 years) and GADA (n = 212; 3.2 years) in children aged ≥2 years. Gestational infections were not associated with the first appearing β-cell autoantibodies overall. However, gestational respiratory infections (G-RI) showed a consistent protective influence on IAA (HR 0.64, 95% CI 0.45-0.91) among CTLA4-(AG, GG) children (G-RI*CTLA4 interaction, p = 0.002). The predominant associations of HLA-DR-DQ 4-8/8-4 with IAA and HLA-DR-DQ 3-2/3-2 with GADA were not observed if a G-RI was reported (G-RI*HLA-DR-DQ interaction, p = 0.03). The role of G-RI may depend on offspring HLA and CTLA-4 alleles and supports a bidirectional trigger for IAA or GADA as a first appearing β-cell autoantibody in early life.

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“…The possibility that transplacental transfer of maternal islet autoantibodies confers an increased risk for type 1 diabetes has been suggested [164] questioned [145,[165][166][167] and discussed in recent reviews [168][169][170]. Even in infants whose mother has diabetes-related autoantibodies, these placentally-transferred autoantibodies almost always fade in infancy, followed by an autoantibody negative period prior to development of autoantibodies usually after age 15 months in young children who subsequently develop T1D [171].…”

Section: Perinatal Factors and Postnatal Growthmentioning

confidence: 98%

Environmental factors in the development of Type 1 diabetes

Peng

Hagopian

2007

Rev Endocr Metab Disord

113

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Environmental factors appear to play an important role in the pathogenesis of childhood-onset type 1 diabetes (T1D). The most important factors are thought to be infectious, dietary, perinatal, and psychosocial. Enteroviruses (especially Coxsackie B virus), breastfeeding, the early presence or lack of certain foods, birth weight, childhood over-nutrition, maternal islet autoimmunity, and negative stress events have been shown to be related to the prevalence of T1D. However, clear conclusions to date are limited because most studies lacked power to detect exposure/disease associations, were not prospective or long-term, did not start in infancy, had imprecise or infrequent exposure estimates, had confounding exposures, and failed to account for genetic susceptibility. In addition to the identification of specific antigenic triggers, several more general hypotheses, including the accelerator and hygiene hypotheses, are testable approaches worth pursuing.

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Islet autoantibodies in cord blood: maternal, fetal, or neither?

Cited by 6 publications

References 43 publications

Cord blood islet autoantibodies and seasonal association with the type 1 diabetes high-risk genotype

Cord blood islet autoantibodies and seasonal association with the type 1 diabetes high-risk genotype

Gestational respiratory infections interacting with offspring HLA and CTLA-4 modifies incident β-cell autoantibodies

Environmental factors in the development of Type 1 diabetes

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