Naturally presented HLA class I–restricted epitopes from the neurotrophic factor S100-β are targets of the autoimmune response in type 1 diabetes
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Título: | Naturally presented HLA class I–restricted epitopes from the neurotrophic factor S100-β are targets of the autoimmune response in type 1 diabetes |
Autor/a: | Calviño Sampedro, Cristina Gómez Touriño, Iria María Cordero Santamaría, Óscar Javier Reche Gallardo, Pedro Antonio Gómez Perosanz, Marta Rodríguez Díaz, Miguel Ángel Sueiro, Aurelio M. Viñuela Roldán, Juan Evaristo Varela Calviño, Rubén |
Centro/Departamento: | Universidade de Santiago de Compostela. Departamento de Bioloxía Funcional Universidade de Santiago de Compostela. Departamento de Bioquímica e Bioloxía Molecular |
Palabras chave: | Cytotoxic lymphocytes | Autoantigen | S100b peptide epitopes | Immunotherapy | Peri-insular Schwann cells | |
Data: | 2019 |
Editor: | Federation of American Societies for Experimental Biology |
Cita bibliográfica: | Calviño-Sampedro, C., Gomez-Tourino, I., Cordero, O., Reche, P., Gómez-Perosanz, M., & Sánchez-Trincado, J. et al. (2019). Naturally presented HLA class I–restricted epitopes from the neurotrophic factor S100-β are targets of the autoimmune response in type 1 diabetes. The FASEB Journal, fj.201802270R. doi: 10.1096/fj.201802270r |
Resumo: | Type 1 diabetes (T1D) results from the destruction of pancreatic β-cells by the immune system, and CD8+ T lymphocytes are critical actors in this autoimmune response. Pancreatic islets are surrounded by a mesh of nervous cells, the peri-insular Schwann cells, which are also targeted by autoreactive T lymphocytes and express specific antigens, such as the neurotrophic factor S100-β. Previous work has shown increased proliferative responses to whole S100-β in both human T1D patients and the nonobese diabetic (NOD) mouse model. We describe for the first time naturally processed and presented epitopes (NPPEs) presented by class I human leukocyte antigen–A*02:01 (A2.1) molecules derived from S100-β. These NPPEs triggered IFN-γ responses more frequently in both newly diagnosed and long-term T1D patients compared with healthy donors. Furthermore, the same NPPEs are recognized during the autoimmune response leading to diabetes in A2.1-transgenic NOD mice as early as 4 wk of age. Interestingly, when these NPPEs are used to prevent diabetes in this animal model, an acceleration of the disease is observed together with an exacerbation in insulitis and an increase in S100-β–specific cytotoxicity in vaccinated animals. Whether these can be used in diabetes prevention needs to be carefully evaluated in animal models before use in future clinical assays.—Calviño-Sampedro, C., Gomez-Tourino, I., Cordero, O. J., Reche, P. A., Gómez-Perosanz, M., Sánchez-Trincado, J. L., Rodríguez, M. Á., Sueiro, A. M., Viñuela, J. E., Calviño, R. V. Naturally presented HLA class I–restricted epitopes from the neurotrophic factor S100-β are targets of the autoimmune response in type 1 diabetes |
Versión do editor: | https://doi.org/10.1096/fj.201802270R |
URI: | http://hdl.handle.net/10347/18515 |
DOI: | 10.1096/fj.201802270R |
ISSN: | 0892-6638 |
E-ISSN: | 1530-6860 |
Dereitos: | © The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International (CC BY 4.0) (http://creativecommons. org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited Atribución 4.0 Internacional |
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© The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International (CC BY 4.0) (http://creativecommons. org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
© The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 International (CC BY 4.0) (http://creativecommons. org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited