The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Autoreactive CD8 T cells associated with β cell destruction in type 1 diabetes
Open accessAbstract
Type 1 diabetes is a T cell-mediated autoimmune disease, and insulin is an important target of the autoimmune response associated with β cell destruction. The mechanism of destruction is still unknown. Here, we provide evidence for CD8 T cell autoreactivity associated with recurrent autoimmunity and loss of β cell function in type 1 diabetic islet transplant recipients. We first identified an insulin B chain peptide (insB10-18) with extraordinary binding affinity to HLA-A2(*0201) that is expressed by the majority of type 1 diabetes patients. We next demonstrated that this peptide is naturally processed by both constitutive and immuno proteasomes and translocated to the endoplasmic reticulum by the peptide transporter TAP1 to allow binding to HLA-A2 in the endoplasmic reticulum and cell surface presentation. Peripheral blood mononuclear cells from a healthy donor were primed in vitro with this peptide, and CD8 T cells were isolated that specifically recognize target cells expressing the insulin B chain peptide. HLA-A2 insB10-18 tetramer staining revealed a strong association between detection of autoreactive CD8 T cells and recurrent autoimmunity after islet transplantation and graft failure in type 1 diabetic patients. We demonstrate that CD8 T cell autoreactivity is associated with β cell destruction in type 1 diabetes in humans.
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Cites
Phenotypic Analysis of Antigen-Specific T Lymphocytes
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Characterization of Peptides Bound to the Class I MHC Molecule HLA-A2.1 by Mass Spectrometry
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Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice
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Prominent role of secondary anchor residues in peptide binding to HLA-A2.1 molecules
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Self-citationEndoplasmic Reticulum Stress and the Development of Diabetes
Harding, H. P., & Ron, D. (2002) · Diabetes · doi:10.2337/diabetes.51.2007.s455 · Cited by 465
The role of T-cells in the pathogenesis of Type 1 diabetes: From cause to cure
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Type 1 Diabetes: Etiology, Immunology, and Therapeutic Strategies
Van Belle, T. L., Coppieters, K. T., & Von Herrath, M. G. (2011) · Physiological Reviews · doi:10.1152/physrev.00003.2010 · Cited by 1,022
Coppieters, K. T., Dotta, F., Amirian, N., Campbell, P. D., Kay, T. W. H., Atkinson, M. A., Roep, B. O., & von Herrath, M. G. (2012) · Journal of Experimental Medicine · doi:10.1084/jem.20111187 · Cited by 672
Self-citationType 1 diabetes mellitus as a disease of the β-cell (do not blame the immune system?)
Roep, B. O., Thomaidou, S., van Tienhoven, R., & Zaldumbide, A. (2021) · Nature Reviews Endocrinology · doi:10.1038/s41574-020-00443-4 · Cited by 623
Self-citationKv1.3 channels are a therapeutic target for T cell-mediated autoimmune diseases
Beeton, C., Wulff, H., Standifer, N. E., Azam, P., Mullen, K. M., Pennington, M. W., Kolski-Andreaco, A., Wei, E., Grino, A., Counts, D. R., et al. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605136103 · Cited by 538
TNF receptor 2 pathway: drug target for autoimmune diseases
Faustman, D., & Davis, M. (2010) · Nature Reviews Drug Discovery · doi:10.1038/nrd3030 · Cited by 446
Metadata
- Authors
- Pinkse, G. G. M., Tysma, O. H. M., Bergen, C. A. M., Kester, M. G. D., Ossendorp, F., van Veelen, P. A., Keymeulen, B., Pipeleers, D., Drijfhout, J. W., & Roep, B. O.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2005-12-09
- Volume
- 102
- Issue
- 51
- Pages
- 18425-18430
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2071591384
- Cited by
- 276
- References
- 42
- FWCI
- 10.08
- Type
- journal article
- Language
- en
- Open access
- green
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- Pinkse, G. G. M., Tysma, O. H. M., Bergen, C. A. M., Kester, M. G. D., Ossendorp, F., van Veelen, P. A., Keymeulen, B., Pipeleers, D., Drijfhout, J. W., & Roep, B. O. (2005). Autoreactive CD8 T cells associated with β cell destruction in type 1 diabetes. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0508621102
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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