Differential association of HLA with three subtypes of type 1 diabetes: fulminant, slowly progressive and acute-onset

Kawabata, Yumiko; Ikegami, Hiroshi; Awata, Takuya; Imagawa, Akihisa; Maruyama, Taro; Kawasaki, Eiji; Tanaka, Shoichiro; Shimada, Akira; Osawa, Haruhiko; Kobayashi, Tetsuro; Hanafusa, Toshiaki; Tokunaga, Katsushi; Makino, Hideichi

doi:10.1007/s00125-009-1539-9

Cited by 127 publications

(136 citation statements)

References 20 publications

(27 reference statements)

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“…The alleles and haplotypes associated with acute-onset and those associated with slowly progressive T1D are similar (14). Hashimoto et al (15) reported that the characteristics of susceptibility HLA haplotypes differed among patients with APS3v (T1D and GD), T1D alone and GD alone.…”

Section: Frequencies Of Antigen or Allele Controlmentioning

confidence: 94%

Simultaneous Occurrence of Type 1 Diabetes Mellitus and Graves' Disease: A Report of Two Cases and a Review of the Literature

et al. 2013

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Two unrelated Japanese women, 41 and 27 years of age, were admitted with histories of thirst, weight loss and palpitations of a few weeks' duration. Both were diagnosed to have diabetic ketosis or ketoacidosis with acute-onset type 1 diabetes (T1D) and Graves' disease (GD) (autoimmune polyglandular syndrome type 3 variant; APS3v), and were treated with intensive insulin therapy and anti-thyroid drugs. Human leukocyte antigen examinations showed that both cases had the HLA-A2, A24, B54, and DRB1*04:05-DQA1*03:03-DQB1*04:01 haplotype, which made them susceptible not only to APS3v, but also to both acute-onset T1D and GD. The genetic background of patients strongly contributes to the simultaneous occurrence of T1D and GD.

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Section: Frequencies Of Antigen or Allele Controlmentioning

confidence: 94%

Simultaneous Occurrence of Type 1 Diabetes Mellitus and Graves' Disease: A Report of Two Cases and a Review of the Literature

et al. 2013

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“…We reported that the HLA-DRB1*04:05-DQB1*04:01 haplotype is associated with Japanese fulminant type 1 diabetes in a homozygous manner [14,15].…”

Section: Enterovirus In the Pancreasmentioning

confidence: 94%

“…These activated antigen-presenting cells could potentially activate preprimed autoreactive T cells, which can then initiate autoimmune response (bystander activation of autoreactive immune T cells) [43]. In addition to this mode of bystander activation of autoreactive T cells, virus-specific T cells are due to abundant lymphoplasmacytic inflammation to the exocrine pancreas [ [15]. The similarity of histological findings and genetic background and the high prevalence of impaired glucose tolerance and autoantibodies against amylase suggest that autoimmune mechanisms against amylase might have some common effects on the destruction of pancreatic islets and exocrine tissues in both fulminant type 1 diabetes and autoimmune pancreatitis.…”

Section: Bystander Activation/killing Of Islet Cells In Fulminant Typmentioning

confidence: 99%

Pathophysiological mechanisms involving aggressive islet cell destruction in fulminant type 1 diabetes [Review]

et al. 2013

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Abstract. Fulminant type 1 diabetes is characterized by a rapid onset of severe hyperglycemia and ketoacidosis, with subsequent poor prognosis of diabetic complications. This review summarizes new findings related to the pathophysiology of accelerated β-cell failure in fulminant type 1 diabetes. Immunohistological examination revealed the presence of enterovirus in pancreatic islet cells and exocrine tissues and hyperexpression of pattern recognition receptors (PRRs) including melanoma differentiation-associated antigen 5 (MDA5), retinoic acid-inducible gene-I (RIG-I), Toll-like receptor (TLR)3 and TLR4, essential sensors of innate immunity, in islet cells and mononuclear cells (MNCs) infiltrating islets. Interferon (IFN)-α and IFN-β, products of PRR cascades, were expressed in both islet cells and infiltrating MNCs. Phenotypes of infiltrating cells around and/or into islets were mainly dendritic cells, macrophages and CD8+ T cells. Islet β-cells simultaneously expressed CXC chemokine ligand 10 (CXCL10), IFN-γ and interleukin-18, indicating that these chemokines/ cytotoxic cytokines mutually amplify their cytoplasmic expression in the islet cells. These positive feedback systems might enhance adaptive immunity, leading to rapid and complete loss of β-cells in fulminant type 1 diabetes. In innate and adaptive/autoimmune immune processes, the mechanisms behind bystander activation/killing might further amplify β-cell destruction. In addition to intrinsic pathway of cell apoptosis, the Fas and Fas ligand pathway are also involved as an extrinsic pathway of cell apoptosis. A high prevalence of anti-amylase autoantibodies was recognized in patients with fulminant type 1 diabetes, which suggests that Th2 T-cell reactive immunity against amylase might contribute to β-cell destruction in fulminant type 1 diabetes.

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“…However the degradation mechanism of cell in FT1DM of humans is unknown. Recently, it has been reported that the onset of FT1DM may be attributed to certain HLA subtype, to viral infection, or to pregnancy (Imagawa et al, 2003;Imagawa et al, 2005;Shimizu et al, 2006;Kawabata et al, 2009). In recent study, macrophages and T cells -but not natural killer cells -had infiltrated the islets and the exocrine pancreas and Toll-like receptor (TLR) 3, a sensor of viral components, was detected in most of macrophages and T cells in FT1DM patients (Shibasaki et al, 2010).…”

Section: Onset Of Fulminant Type 1 Diabetes Mellitusmentioning

confidence: 99%

“…Insulitis with macrophage dominant infiltration was observed in IRS-2 deficient mice and human FT1DM. Destruction mechanism of cells associated HLA, viral infection and pregnancy were investigated in detail in human FT1DM patients (Kawabata et al, 2009;Murabayashi et al, 2009;Tan & Loh, 2010), whereas association with MHC was not investigated in IRS-2 deficient mice. Since FT1DM was observed in only male IRS-2 deficient mice, pregnancy is not associated with onset of FT1DM.…”

Section: Comparison Of Pathology Of Ft1dm Between Irs-2 Deficient Micmentioning

confidence: 99%

Fulminant Type 1 Diabetes Mellitus in IRS-2 Deficient Mice

Arai¹,

Mori²,

Hashimoto³

2011

Type 1 Diabetes - Complications, Pathogenesis, and Alternative Treatments

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Differential association of HLA with three subtypes of type 1 diabetes: fulminant, slowly progressive and acute-onset

Cited by 127 publications

References 20 publications

Simultaneous Occurrence of Type 1 Diabetes Mellitus and Graves' Disease: A Report of Two Cases and a Review of the Literature

Simultaneous Occurrence of Type 1 Diabetes Mellitus and Graves' Disease: A Report of Two Cases and a Review of the Literature

Pathophysiological mechanisms involving aggressive islet cell destruction in fulminant type 1 diabetes [Review]

Fulminant Type 1 Diabetes Mellitus in IRS-2 Deficient Mice

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