Genes Mediating Environment Interactions in Type 1 Diabetes

Biroš, Erik; Jordan, Margaret A.; Baxter, Alan G.

doi:10.1900/rds.2005.2.192

Cited by 12 publications

(11 citation statements)

References 238 publications

(200 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similarly, strategies to target autoantigens to immature, steady-state dendritic cells could guide the immune reIntroduction ype 1 diabetes (T1D) is a complex organspecific autoimmune disease involving defects in immunoregulation. The disease has a relatively strong genetic association, and multiple environmental risk factors are involved in triggering its onset [1]. Different microbes, and chemical and dietary factors have been implicated either individually or in combination in causing autoimmunity to islet β-cells.…”

Section: ■ Abstractmentioning

confidence: 99%

Genetic Susceptibility to Type 1 Diabetes in the Intracellular Pathway of Antigen Processing – A Subject Review and Cross-Study Comparison

Sia

Weinem²

2005

Rev Diab Stud

View full text Add to dashboard Cite

■ AbstractThe onset and development of type 1 diabetes (T1D) occurs in genetically predisposed individuals, and is attributed to autoimmune destruction of pancreatic β-cells involving a multitude of immune mechanisms. Defects in immune regulation may play a central role in T1D, involving impaired function and communication of both myeloid and lymphoid cells of the innate and adaptive immune compartments. Dendritic cells and regulatory T (Treg) cells are part of this network, which seem to be hampered in their quest to control and regulate tissue-destructive autoimmunity. Recent studies have shown that in vivo activated CD16 -blood monocytes exhibiting proinflammatory features are present in diabetic subjects. These monocytes may govern T cellmediated immune responses towards the development of tissue-destructive Th1 and Th17 subtypes, and give rise to inflammatory macrophages in tissues. Differential effects of cytokines IFN-γ and IL-4 in the development of inflammatory macrophages, and the distinct developmental pathways of proinflammatory or tissue-repair-associated monocytes suggest that controlling the activity of these monocytes could be part of an immune intervention strategy to prevent T1D. Similarly, strategies to target autoantigens to immature, steady-state dendritic cells could guide the immune response away from Th1 and Th17 immune effectors. This review examines potential approaches to this goal by manipulation of myeloid and lymphoid cell regulatory networks in T1D.

show abstract

Section: ■ Abstractmentioning

confidence: 99%

Genetic Susceptibility to Type 1 Diabetes in the Intracellular Pathway of Antigen Processing – A Subject Review and Cross-Study Comparison

Sia

Weinem²

2005

Rev Diab Stud

View full text Add to dashboard Cite

show abstract

“…Identification of genes predisposing to type 1 diabetes is important in establishing effective methods for disease prediction, prevention and intervention. Type 1 diabetes, however, is a multifactorial disease caused by a complex interaction of genetic and environmental factors, with the former consisting of multiple susceptibility genes, which makes identification of disease-causing variants very difficult [4].…”

mentioning

confidence: 99%

Genetic Basis of Type 1 Diabetes: Similarities and Differences between East and West

Ikegami

Noso²,

Babaya³

et al. 2008

Rev Diabet Stud

View full text Add to dashboard Cite

“…The complexity of the genetics of autoimmune traits has significantly impeded the fine localization and identification of disease susceptibility genes [41,42]. We have attempted to overcome this problem by studying subphenotypes that contribute to the etiology of diabetes, and potentially many other autoimmune diseases, such as defects in immunoregulation [43].…”

Section: Discussionmentioning

confidence: 99%

Allelic Variation of Ets1 Does Not Contribute to NK and NKT Cell Deficiencies in Type 1 Diabetes Susceptible NOD Mice

Jordan

Poulton²,

Fletcher³

et al. 2009

Rev Diabet Stud

Self Cite

View full text Add to dashboard Cite

■ AbstractThe NOD mouse strain is a well characterized model of type 1 diabetes that shares several of the characteristics of Ets1-deficient targeted mutant mice, viz: defects in TCR allelic exclusion, susceptibility to a lupus like disease characterized by IgM and IgG autoantibodies and immune complexmediated glomerulonephritis, and deficiencies of NK and NKT cells. Here, we sought evidence for allelic variation of Ets1 in mice contributing to the NK and NKT cell phenotypes of the NOD strain. ETS1 expression in NK and NKT cells was reduced in NOD mice, compared to C57BL/6 mice. Although NKT cells numbers were significantly correlated with ETS1 expression in both strains, NKT cell numbers were not linked to the Ets1 gene in a first backcross from NOD to C57BL/6 mice. These results indicate that allelic variation of Ets1 did not contribute to variation in NKT cell numbers in these mice. It remains possible that a third factor not linked to the Ets1 locus controls both ETS1 expression and subsequently NK and NKT cell phenotypes.

show abstract

Genes Mediating Environment Interactions in Type 1 Diabetes

Cited by 12 publications

References 238 publications

Genetic Susceptibility to Type 1 Diabetes in the Intracellular Pathway of Antigen Processing – A Subject Review and Cross-Study Comparison

Genetic Susceptibility to Type 1 Diabetes in the Intracellular Pathway of Antigen Processing – A Subject Review and Cross-Study Comparison

Genetic Basis of Type 1 Diabetes: Similarities and Differences between East and West

Allelic Variation of Ets1 Does Not Contribute to NK and NKT Cell Deficiencies in Type 1 Diabetes Susceptible NOD Mice

Contact Info

Product

Resources

About