Abstract
Type 1 diabetes (T1D) is an autoimmune disease, in which pancreatic cells are destroyed in genetically predisposed individuals. While the direct contribution of autoantibodies to the disease pathogenesis is controversial, it is generally recognised that the mechanism of cell destruction is mediated by autoreactive T cells that had escaped the thymic selection. We aimed to design a method to detect circulating CD8+ T cells autoreactive against an epitope of the glutamic acid decarboxylase autoantigen, isoform 65 (GAD65) ex vivo in T1D patients by using HLA class I tetramers. Low frequencies of GAD65 peptide-specific CD8+ cytotoxic T lymphocytes were detected in peripheral blood lymphocytes (PBMC) of normal controls after GAD65 peptide-specific stimulation. Conversely, their frequencies were significantly higher than in controls in PBMC of T1D patients after GAD65 peptide stimulation. These preliminary data are encouraging in order to develop a reliable assay to be employed in large-scale screening studies.
| Original language | English |
|---|---|
| Article number | 576219 |
| Journal | Journal of Biomedicine and Biotechnology |
| Volume | 2009 |
| DOIs | |
| Publication status | Published - 2009 |
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ASJC Scopus subject areas
- Biotechnology
- Molecular Medicine
- Genetics
- Molecular Biology
- Health, Toxicology and Mutagenesis
- Medicine(all)
Cite this
Detection of GAD65 autoreactive t-cells by HLA class i tetramers in type 1 diabetic patients. / Fierabracci, Alessandra; Giuliani, Laura; Mele, Raffaella; Di Giovine, Monica; Altieri, Laura; Crinó, Antonino; Ravá, Lucilla.
In: Journal of Biomedicine and Biotechnology, Vol. 2009, 576219, 2009.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Detection of GAD65 autoreactive t-cells by HLA class i tetramers in type 1 diabetic patients
AU - Fierabracci, Alessandra
AU - Giuliani, Laura
AU - Mele, Raffaella
AU - Di Giovine, Monica
AU - Altieri, Laura
AU - Crinó, Antonino
AU - Ravá, Lucilla
PY - 2009
Y1 - 2009
N2 - Type 1 diabetes (T1D) is an autoimmune disease, in which pancreatic cells are destroyed in genetically predisposed individuals. While the direct contribution of autoantibodies to the disease pathogenesis is controversial, it is generally recognised that the mechanism of cell destruction is mediated by autoreactive T cells that had escaped the thymic selection. We aimed to design a method to detect circulating CD8+ T cells autoreactive against an epitope of the glutamic acid decarboxylase autoantigen, isoform 65 (GAD65) ex vivo in T1D patients by using HLA class I tetramers. Low frequencies of GAD65 peptide-specific CD8+ cytotoxic T lymphocytes were detected in peripheral blood lymphocytes (PBMC) of normal controls after GAD65 peptide-specific stimulation. Conversely, their frequencies were significantly higher than in controls in PBMC of T1D patients after GAD65 peptide stimulation. These preliminary data are encouraging in order to develop a reliable assay to be employed in large-scale screening studies.
AB - Type 1 diabetes (T1D) is an autoimmune disease, in which pancreatic cells are destroyed in genetically predisposed individuals. While the direct contribution of autoantibodies to the disease pathogenesis is controversial, it is generally recognised that the mechanism of cell destruction is mediated by autoreactive T cells that had escaped the thymic selection. We aimed to design a method to detect circulating CD8+ T cells autoreactive against an epitope of the glutamic acid decarboxylase autoantigen, isoform 65 (GAD65) ex vivo in T1D patients by using HLA class I tetramers. Low frequencies of GAD65 peptide-specific CD8+ cytotoxic T lymphocytes were detected in peripheral blood lymphocytes (PBMC) of normal controls after GAD65 peptide-specific stimulation. Conversely, their frequencies were significantly higher than in controls in PBMC of T1D patients after GAD65 peptide stimulation. These preliminary data are encouraging in order to develop a reliable assay to be employed in large-scale screening studies.
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U2 - 10.1155/2009/576219
DO - 10.1155/2009/576219
M3 - Article
VL - 2009
JO - Journal of Biomedicine and Biotechnology
JF - Journal of Biomedicine and Biotechnology
SN - 1110-7243
M1 - 576219
ER -