Islet Cell Antibodies in Children With Mumps Infection

Helmke, K.; Otten, A; Willems, Wulf R.

doi:10.1016/s0140-6736(80)90105-1

Cited by 83 publications

(30 citation statements)

References 6 publications

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“…Fourth, viruses [84,85] and virus-specific antibodies [86][87][88][89] can be detected in newly diagnosed patients with T1D. Indeed, a number of viruses have been associated with T1D in humans, including rubella [90], mumps [91,92], CMV [93,94], EBV [95,96], varicella zoster [97], retroviruses [98,99], rotavirus [100], and coxsackie B virus [71,[101][102][103][104]. The most convincing evidence published so far implicates coxsackie B viruses in triggering diabetes.…”

Section: Viruses and T1dmentioning

confidence: 99%

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

Lien¹,

Zipris²

2009

CMM

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Toll-like receptors (TLRs) and the innate immune system play a key role in sensing and eliminating microbial infections. Interactions between TLRs and their ligands expressed by microbial pathogens induce a cascade of intracellular signaling events, culminating in the upregulation of proinflammatory pathways. Over the past two decades, numerous studies have established the role of the acquired immune system in the mechanism triggering type 1 diabetes (T1D). The recent discovery of TLRs has led to the recognition that the innate immune system may act, under some circumstances, as a double-edged sword. In addition to its beneficial role in host defense, it may lead to upregulation of proinflammatory autoimmune responses, islet destruction and diabetes. Indeed, recent observations are consistent with the hypothesis that altered innate functions exist in patients with T1D and could be part of the mechanism leading to disease onset, but the underlying mechanisms and the relevance of these alterations to early events triggering disease remain to be identified. Data obtained from mouse and rat models of T1D implicated TLR pathways in both disease induction and prevention. In both the NOD mouse and diabetes-prone BB (BBDP) rat, TLR upregulation can suppress disease. In the BioBreeding Diabetes Resistant (BBDR) rat, however, diabetes induced by virus infection involves the upregulation of TLR9 pathways, and generic TLR upregulation synergizes with virus infection on diabetes induction. Studies performed in mouse models of T1D with spontaneous or induced T1D implicate TLR1, TLR2, TLR3, and TLR7 in disease mechanisms. The finding that TLR pathways are involved in mediating islet inflammation holds great promise for identifying new molecules that could potentially be targeted to specifically suppress the autoimmune process in individuals at high risk for disease development. The potential link between TLR upregulation and autoimmunity emphasizes the need for caution in using new therapies involving TLR agonists as vaccine adjuvants.

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Section: Viruses and T1dmentioning

confidence: 99%

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

Lien¹,

Zipris²

2009

CMM

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“…An early observation was the association of congenital rubella infection with a very high rate of subsequent T1D [39]. Subsequently, other human viruses were reported to be associated with human T1D, including but not limited to Coxsackie B virus [40,41], mumps [42], echovirus [43,44], cytomegalovirus [45][46][47], Epstein-Barr virus (EBV) [48,49], retrovirus [50], rotavirus [51] and parvovirus B19 [52,53].…”

Section: Infectious Agents Including Virusesmentioning

confidence: 99%

Environmental factors in the development of Type 1 diabetes

Peng

Hagopian

2007

Rev Endocr Metab Disord

112

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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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Section: Mumps Virusmentioning

confidence: 99%

“…Mumps virus was one of the first viruses implicated in the development of human T1D; several cases were reported in which mumps infection appeared to precede the onset of T1D [30,31]. It has been hypothesized that infection with mumps virus may induce autoimmunity, as some children appear to develop islet cell autoantibodies during parotiditis [31], however the mechanisms by which this might occur are unknown. In vitro studies have shown that human beta cells could be infected with mumps virus [88], that mumps infection of a human insulinoma cell line induced the release of IL-1 and IL-6 and upregulated the expression of HLA class I and II anti- Figure 3 Schematic diagram of the possible mechanism for KRV-induced diabetes in DR-BB rats.…”

Section: Mumps Virusmentioning

confidence: 99%

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A New Look at Viruses in Type 1 Diabetes

Jun¹,

Yoon²

2004

ILAR Journal

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Type 1 diabetes results from the destruction of pancreatic beta cells. Genetic factors are believed to be a major component for the development of type 1diabetes, but the concordance rate for the development of diabetes in identical twins is only about 40%, suggesting that non-genetic factors play an important role in the expression of the disease. Viruses are one environmental factor that is implicated in the pathogenesis of type 1 diabetes. To date, 14 different viruses have been reported to be associated with the development of type 1 diabetes in humans and animal models. Viruses may be involved in the pathogenesis of type 1 diabetes in at least two distinct ways: by inducing beta cellspecific autoimmunity, with or without infection of the beta cells, (e.g. Kilham rat virus) and by cytolytic infection and destruction of the beta cells (e.g. encephalomyocarditis virus in mice). With respect to virus-mediated autoimmunity, retrovirus, reovirus, Kilham rat virus, bovine viral diarrhoea-mucosal disease virus, mumps virus, rubella virus, cytomegalovirus and Epstein-Barr virus are discussed. With respect to the destruction of beta cells by cytolytic infection, encephalomyocarditis virus, mengovirus and Coxsackie B viruses are discussed. In addition, a review of transgenic animal models for virus-induced autoimmune diabetes is included, particularly with regard to lymphocytic choriomeningitis virus, influenza viral proteins and the EpsteinBarr viral receptor. Finally, the prevention of autoimmune diabetes by infection of viruses such as lymphocytic choriomeningitis virus is discussed.

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Islet Cell Antibodies in Children With Mumps Infection

Cited by 83 publications

References 6 publications

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

Environmental factors in the development of Type 1 diabetes

A New Look at Viruses in Type 1 Diabetes

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