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- W1949665260 abstract "Summary Type 1 diabetes results from destruction of insulin-producing beta cells in pancreatic islets and is characterized by islet cell autoimmunity. Autoreactivity against non-beta cell-specific antigens has also been reported, including targeting of the calcium-binding protein S100β. In preclinical models, reactivity of this type is a key component of the early development of insulitis. To examine the nature of this response in type 1 diabetes, we identified naturally processed and presented peptide epitopes derived from S100β, determined their affinity for the human leucocyte antigen (HLA)-DRB1*04:01 molecule and studied T cell responses in patients, together with healthy donors. We found that S100β reactivity, characterized by interferon (IFN)-γ secretion, is a characteristic of type 1 diabetes of varying duration. Our results confirm S100β as a target of the cellular autoimmune response in type 1 diabetes with the identification of new peptide epitopes targeted during the development of the disease, and support the preclinical findings that autoreactivity against non-beta cell-specific autoantigens may have a role in type 1 diabetes pathogenesis." @default.
- W1949665260 created "2016-06-24" @default.
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- W1949665260 date "2015-04-14" @default.
- W1949665260 modified "2023-09-27" @default.
- W1949665260 title "Characterization of the autoimmune response against the nerve tissue S100β in patients with type 1 diabetes" @default.
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- W1949665260 doi "https://doi.org/10.1111/cei.12572" @default.
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