The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Defective Suppressor Function in CD4+CD25+ T-Cells From Patients With Type 1 Diabetes
Open accessAbstract
Type 1 diabetes is a T-cell–mediated disease that is associated with loss of immunological tolerance to self-antigens. The mechanisms involved in maintenance of peripheral tolerance include a specialized subset of regulatory T-cells (Treg) within the CD4+CD25+ T-cell population, but the function and phenotype of these cells in type 1 diabetes have not been investigated. We hypothesized that a deficiency in the CD4+CD25+ Treg population or its function could contribute to the lack of self-tolerance evident in patients with type 1 diabetes. We show that although levels of CD4+CD25+ T-cells are normal in patients with recent-onset adult type 1 diabetes, the ability of the Tregs in this population to suppress T-cell proliferation during in vitro cocultures is markedly reduced compared with control subjects (P = 0.007). Moreover, in patients with type 1 diabetes, these cocultures display a more proinflammatory phenotype, with increased secretion of interferon-γ (P = 0.005) and decreased interleukin-10 production (P = 0.03). These deficiencies may reflect a disturbance in the balance of the CD4+CD25+ population, because in patients with type 1 diabetes, a higher proportion of these cells coexpress the early activation marker CD69 (P = 0.007) and intracellular CTLA-4 (P = 0.01). These data demonstrate deficiency in function of the CD4+CD25+ Treg population that may influence the pathogenesis of type 1 diabetes.
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Cites
Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease
Ueda, H., Howson, J. M. M., Esposito, L., Heward, J., Snook, Chamberlain, G., Rainbow, D. B., Hunter, K. M. D., Smith, A. N., Di Genova, G., et al. (2003) · Nature · doi:10.1038/nature01621 · Cited by 2,175
Anti-CD3 monoclonal antibody in new-onset type 1 diabetes mellitus
Herold, K. C., Hagopian, W., Auger, J. A., Poumian-Ruiz, E., Taylor, L., Donaldson, D., Gitelman, S. E., Harlan, D. M., Xu, D., Zivin, R. A., et al. (2002) · New England Journal of Medicine · doi:10.1056/nejmoa012864 · Cited by 1,222
CTLA-4: new insights into its biological function and use in tumor immunotherapy
Egen, J. G., Kuhns, M. S., & Allison, J. P. (2002) · Nature Immunology · doi:10.1038/ni0702-611 · Cited by 940
CD80 (B7-1) Binds Both CD28 and CTLA-4 with a Low Affinity and Very Fast Kinetics
van der Merwe, P. A., Bodian, D. L., Daenke, S., Linsley, P., & Davis, S. J. (1997) · The Journal of Experimental Medicine · doi:10.1084/jem.185.3.393 · Cited by 551 · cited 1×
“CTLA-4 is a negative regulator of T-cell activation pathways (40,41) expressed de novo after T-cell activation and is considered to constitute part of a physiological postactivation negative feedback pathway in T-cell homeostasis (42).”
BackgroundFeutren, G., Assan, R., Karsenty, G., Du Rostu, H., Sirmai, J., Papoz, L., Vialettes, B., Vexiau, P., Rodier, M., Lallemand, A., et al. (1986) · The Lancet · doi:10.1016/s0140-6736(86)91943-4 · Cited by 448
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The PD‐1 pathway in tolerance and autoimmunity
Francisco, L. M., Sage, P. T., & Sharpe, A. H. (2010) · Immunological Reviews · doi:10.1111/j.1600-065x.2010.00923.x · Cited by 2,300
Risk Alleles for Multiple Sclerosis Identified by a Genomewide Study
(2007) · New England Journal of Medicine · doi:10.1056/nejmoa073493 · Cited by 1,746
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Campbell, D. J., & Koch, M. A. (2011) · Nature Reviews Immunology · doi:10.1038/nri2916 · Cited by 773
Central Role of Defective Interleukin-2 Production in the Triggering of Islet Autoimmune Destruction
Tang, Q., Adams, J. Y., Penaranda, C., Melli, K., Piaggio, E., Sgouroudis, E., Piccirillo, C. A., Salomon, B. L., & Bluestone, J. A. (2008) · Immunity · doi:10.1016/j.immuni.2008.03.016 · Cited by 729
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Dominguez-Villar, M., & Hafler, D. A. (2018) · Nature Immunology · doi:10.1038/s41590-018-0120-4 · Cited by 713
Metadata
- Authors
- Lindley, S., Dayan, C. M., Bishop, A., Roep, B. O., Peakman, M., & Tree, T. I. M.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-01-01
- Volume
- 54
- Issue
- 1
- Pages
- 92-99
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2083826829
- Cited by
- 861
- References
- 5
- FWCI
- 22.21
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Lindley, S., Dayan, C. M., Bishop, A., Roep, B. O., Peakman, M., & Tree, T. I. M. (2005). Defective Suppressor Function in CD4+CD25+ T-Cells From Patients With Type 1 Diabetes. Diabetes. https://doi.org/10.2337/diabetes.54.1.92
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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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