Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand and CD56 Expression in Patients With Type 1 Diabetes Mellitus

Cheung, S.C.; Metzger, Daniel L.; Wang, Xiaojie; Huang, Junqi; Tai, Joseph; Tingle, Aubrey J.; Ou, Dawei

doi:10.1097/01.mpa.0000148515.77497.4b

Cited by 22 publications

(15 citation statements)

References 43 publications

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“…TRAIL has also been associated with diabetes, with many reports claiming a destructive role in disease progression, as well as a protective role suggested by yet many other studies [23,24]. In accordance with the claimed protective role, newly diagnosed, non-drug using T2D patients had lower levels of circulating sTRAIL compared to healthy individuals in a previous study by our group [25].…”

Section: Discussionsupporting

confidence: 80%

Association of circulating sTRAIL and high-sensitivity CRP with type 2 diabetic nephropathy and foot ulcers

et al. 2013

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BackgroundHyperglycemia is among the potent factors that may induce or facilitate apoptosis. TNF-Related Apoptosis-Inducing Factor (TRAIL) is known for its apoptotic and immunomodulatory effects that have recently been correlated with diabetes. We examined serum-soluble TRAIL (sTRAIL) and high-sensitivity CRP (hs-CRP) levels and their association with various distinct parameters in type 2 diabetic nephropathy patients with diabetic foot disease.Material/MethodsTwenty-two diabetic nephropathy patients with foot ulcers were enrolled in our study. Patients had been diagnosed with diabetes at age 24±10.58 years. Circulating sTRAIL and Hs-CRP levels were compared with control values, and possible correlations were investigated with parameters such as age, Wagner’s Grade (WG), BMI, HbA1c, and creatinine.ResultsSerum sTRAIL levels were significantly reduced in the patient group, compared to healthy subjects. High HsCRP levels correlated with age, and WGS correlated with BMI and creatinine levels.ConclusionsSignificantly suppressed sTRAIL levels in diabetic nephropathy patients with foot ulcers compared to healthy controls suggest a protective role for TRAIL in the disease setting.

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Section: Discussionsupporting

confidence: 80%

Association of circulating sTRAIL and high-sensitivity CRP with type 2 diabetic nephropathy and foot ulcers

et al. 2013

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“…Interestingly, increased TRAIL expression was observed in the infiltrating immune cells of pancreatic islets in patients with type 1 diabetes. 39 Thus, under normal circumstances, Langerhans islets are expected to be protected from the immunemediated attacks through TRAIL expression and from death ligandYmediated apoptosis by way of decoy receptor expression. 40 Because Langerhans islets of PDAC patients exhibited higher DcR2 expression compared with noncancer patients, it would be interesting to see if these patients are more resistant to developing type 1 diabetes compared with noncancer patients.…”

Section: Discussionmentioning

confidence: 99%

High TRAIL Death Receptor 4 and Decoy Receptor 2 Expression Correlates With Significant Cell Death in Pancreatic Ductal Adenocarcinoma Patients

Şanlioğlu¹,

Dirice²,

Elpek³

et al. 2009

Pancreas

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“…In accordance with this, transgenic expression of soluble TNF receptor prevented autoimmune diabetes in NOD mice [Hunger et al, 1997]. Since infiltrating cells of the pancreatic islets displayed elevated levels of TRAIL expression in patients with type 1 diabetes [Cheung et al, 2005], these cells might well use TRAIL death ligand in the destruction of beta cells. Conversely, it is expected that exogenous TRAIL over-expression might protect pancreatic islets from CTL invasion, as depicted on Figure 3.…”

Section: Is Over-expression Of Death Ligands Of Tnf Super Family a VImentioning

confidence: 68%

“…Freshly isolated T cells do not express TRAIL unless they are treated with the type I interferon or CD3 ligation [Kayagaki et al, 1999]. This was further confirmed by the studies showing an increased expression of TRAIL in the infiltrating cells of the pancreatic islets in patients with type 1 diabetes [Cheung et al, 2005]. Intriguingly, TNF and IFN-g treatment upregulated TRAIL gene expression in pancreatic islets of NOD mice but still TRAIL failed to induce apoptosis of freshly isolated pancreatic islets [Mi et al, 2003].…”

Section: Molecular Evidences Connecting Trail Signaling To Autoimmunementioning

confidence: 68%

Molecular mechanisms of death ligand‐mediated immune modulation: A gene therapy model to prolong islet survival in type 1 diabetes

Şanlioğlu

Griffith

Omer

et al. 2008

J of Cellular Biochemistry

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Type 1 diabetes results from the T cell-mediated destruction of pancreatic beta cells. Islet transplantation has recently become a potential therapeutic approach for patients with type 1 diabetes. However, islet-graft failure appears to be a challenging issue to overcome. Thus, complementary gene therapy strategies are needed to improve the islet-graft survival following transplantation. Immune modulation through gene therapy represents a novel way of attacking cytotoxic T cells targeting pancreatic islets. Various death ligands of the TNF family such as FasL, TNF, and TNF-Related Apoptosis-Inducing Ligand (TRAIL) have been studied for this purpose. The over-expression of TNF or FasL in pancreatic islets exacerbates the onset of type 1 diabetes generating lymphocyte infiltrates responsible for the inflammation. Conversely, the lack of TRAIL expression results in higher degree of islet inflammation in the pancreas. In addition, blocking of TRAIL function using soluble TRAIL receptors facilitates the onset of diabetes. These results suggested that contrary to what was observed with TNF or FasL, adenovirus mediated TRAIL gene delivery into pancreatic islets is expected to be therapeutically beneficial in the setting of experimental models of type 1 diabetes. In conclusion; this study mainly reveals the fundamental principles of death ligand-mediated immune evasion in diabetes mellitus.

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Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand and CD56 Expression in Patients With Type 1 Diabetes Mellitus

Abstract: The presence of TRAIL and CD56 markers is part of the T-cell response repertoire in beta-cell destruction.

Cited by 22 publications

References 43 publications

Association of circulating sTRAIL and high-sensitivity CRP with type 2 diabetic nephropathy and foot ulcers

Association of circulating sTRAIL and high-sensitivity CRP with type 2 diabetic nephropathy and foot ulcers

High TRAIL Death Receptor 4 and Decoy Receptor 2 Expression Correlates With Significant Cell Death in Pancreatic Ductal Adenocarcinoma Patients

Molecular mechanisms of death ligand‐mediated immune modulation: A gene therapy model to prolong islet survival in type 1 diabetes

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