Prevention of Type 1 Diabetes: Past Experiences and Future Opportunities

Beik, Przemysław; Ciesielska, Martyna; Kucza, Maria; Kurczewska, Alicja; Kuźmińska, Joanna; Maćkowiak, Bartosz; Niechciał, Elżbieta

doi:10.3390/jcm9092805

Cited by 13 publications

(8 citation statements)

References 87 publications

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“…It is often associated with other autoimmune diseases, first among all T1D. With T1D, CD shares genes conferring risk (both HLA and non HLA) (47) and immunological mechanisms inducing damage at the target tissue (intestinal mucosa or pancreatic islets). Lessons from what implemented for T1D prevention may be particularly useful for CD.…”

Section: Halting the Progression Of Cd: Analogies With Type 1 Diabetesmentioning

confidence: 99%

“…Lessons from what implemented for T1D prevention may be particularly useful for CD. Also for T1D the target population for primary prevention trials is individuals who carry high risk genotypes before the first appearance of islet autoantibodies and also for T1D these trials include mostly low risk dietary interventions such as the avoidance of cow's milk or gluten and the supplementation of n-3 fatty acids or vitamin D (47). The results of these trials have been so far quite disappointing.…”

Section: Halting the Progression Of Cd: Analogies With Type 1 Diabetesmentioning

confidence: 99%

“…Most of the efforts in T1D have been so far directed to slow or to halt the progressive beta cell destruction. Nicotinamide, antigen-specific immune therapy (oral and nasal insulin, GAD alum), monoclonal antibodies, immunosuppressive drugs, hydroycloroquine and anti-inflammatory agents have been tested (47). Particularly promising is the use of monoclonal antibody to CD3 (Tepluzimab) targeting CD8+ cells responsible of beta cell destruction in T1D (49).…”

Section: Halting the Progression Of Cd: Analogies With Type 1 Diabetesmentioning

confidence: 99%

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Can Celiac Disease Be Prevented?

Auricchio¹,

Troncone²

2021

Front. Immunol.

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Celiac disease (CD) is an autoimmune disorder triggered by gluten in genetically susceptible individuals characterized by a variable combination of gluten-dependent symptoms, presence of specific autoantibodies and enteropathy. The health burden of CD is considerable, as it reduces quality of life and, at a societal level, has extensive negative economic consequences. Prevention strategies are based on the identification of at-risk subjects and identification and elimination of risk factors. A number of prospective observational and interventional studies conducted on the general population, and more often in subjects at-risk, have given important information on the natural history of the disease. Both genetic and environmental factors have been identified with the former, in particular histocompatibility genes, playing a major role. Environmental factors, some operating already before birth, have been identified, with feeding pattern in the first year of life (breast feeding, amount and time of introduction of gluten) and infections being the most relevant. Prospective studies have also allowed the identification of biomarkers predictive of the disease which in perspective could better define the population on which to intervene. Interventions have been so far limited to modifications of feeding patterns. However, as also learnt from diseases that share with CD genetic risk factors and mechanisms of damage, such as type 1 diabetes (T1D), future strategies may be envisaged based on protection from infections, manipulation of microbiota, intervention on T cells.

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Section: Halting the Progression Of Cd: Analogies With Type 1 Diabetesmentioning

confidence: 99%

Section: Halting the Progression Of Cd: Analogies With Type 1 Diabetesmentioning

confidence: 99%

Section: Halting the Progression Of Cd: Analogies With Type 1 Diabetesmentioning

confidence: 99%

See 1 more Smart Citation

Can Celiac Disease Be Prevented?

Auricchio¹,

Troncone²

2021

Front. Immunol.

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“…Approximately 70-95% of β-cells are usually lost at the onset of symptoms resulting in reduced pancreas size, although in some individuals a 40% reduction is adequate to elicit symptoms [2,16,27]. Efforts to preserve any residual β-cell function (measured by C-peptide production) using immune intervention therapies have had limited success [28][29][30][31][32]. Notably, only 15% of children displaying single IA positivity progress to T1D [33], and conversely, only 10% of individuals with T1D display single IA positivity [16].…”

Section: Islet Autoimmunitymentioning

confidence: 99%

Viruses and Type 1 Diabetes: From Enteroviruses to the Virome

Isaacs¹,

Foskett²,

Maxwell³

et al. 2021

Preprint

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For over a century, viruses have left a long trail of evidence implicating them as frequent suspects in the development of type 1 diabetes. Through vigorous interrogation of viral infections in individuals with islet autoimmunity and type 1 diabetes using serological and molecular virus detection methods, and mechanistic studies of virus infected human pancreatic β-cells, the prime suspects have been narrowed down to predominantly human enteroviruses. Here we provide a comprehensive overview of evidence supporting the hypothesised role of enteroviruses in the development of islet autoimmunity and type 1 diabetes. We also discuss concerns over the historical focus and investigation bias toward enteroviruses, and summarise current unbiased efforts aimed at characterising the complete population of viruses (the “virome”) contributing early in life to the development of islet autoimmunity and type 1 diabetes. Finally, we review the range of vaccine and antiviral drug candidates currently being evaluated in clinical trials for the prevention and potential treatment of type 1 diabetes.

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“…In T1DM, there is destruction of β -cells and little or no insulin is produced [ 11 , 12 ]. Viruses also seem to induce type 1 diabetes mellitus (T1DM) via molecular mimicry mechanism [ 13 , 14 , 15 ].…”

Section: Introduction-diabetes As a Diseasementioning

confidence: 99%

Maintaining Digestive Health in Diabetes: The Role of the Gut Microbiome and the Challenge of Functional Foods

et al. 2021

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Over the last decades, the incidence of diabetes has increased in developed countries and beyond the genetic impact, environmental factors, which can trigger the activation of the gut immune system, seem to affect the induction of the disease process. Since the composition of the gut microbiome might disturb the normal interaction with the immune system and contribute to altered immune responses, the restoration of normal microbiota composition constitutes a new target for the prevention and treatment of diabetes. Thus, the interaction of gut microbiome and diabetes, focusing on mechanisms connecting gut microbiota with the occurrence of the disorder, is discussed in the present review. Finally, the challenge of functional food diet on maintaining intestinal health and microbial flora diversity and functionality, as a potential tool for the onset inhibition and management of the disease, is highlighted by reporting key animal studies and clinical trials. Early onset of the disease in the oral cavity is an important factor for the incorporation of a functional food diet in daily routine.

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Prevention of Type 1 Diabetes: Past Experiences and Future Opportunities

Cited by 13 publications

References 87 publications

Can Celiac Disease Be Prevented?

Can Celiac Disease Be Prevented?

Viruses and Type 1 Diabetes: From Enteroviruses to the Virome

Maintaining Digestive Health in Diabetes: The Role of the Gut Microbiome and the Challenge of Functional Foods

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