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Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes
Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of pancreatic beta cells. Eosinophils are found in pancreatic tissue from individuals with T1D. Eosinophilic suppression of T cells is dependent of the protein galectin-10. Little is known when it comes to the role...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10199897/ https://www.ncbi.nlm.nih.gov/pubmed/37210405 http://dx.doi.org/10.1038/s41598-023-35300-7 |
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author | Larsson, Helen Albinsson Högberg, Sofie Lind, Marcus Rabe, Hardis Lingblom, Christine |
author_facet | Larsson, Helen Albinsson Högberg, Sofie Lind, Marcus Rabe, Hardis Lingblom, Christine |
author_sort | Larsson, Helen |
collection | PubMed |
description | Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of pancreatic beta cells. Eosinophils are found in pancreatic tissue from individuals with T1D. Eosinophilic suppression of T cells is dependent of the protein galectin-10. Little is known when it comes to the role of eosinophil granulocytes in type 1 diabetes. Here we show that individuals with long-standing T1D had lower levels of galectin-10(hi) eosinophils and a subgroup of galectin-10(hi) eosinophils were entirely absent in all T1D patients. In addition, 7% immature eosinophils were present in the circulation of T1D patients whereas 0.8% in healthy individuals. Furthermore, higher levels of CD4+CD8+ T cells and Th17 cells were observed in patients with T1D. Blood samples from 12 adult individuals with long-standing T1D and 12 healthy individuals were compared using cytometry by time-of-flight. Lower levels of galectin-10(hi) eosinophils, which are potent T cell suppressors, in individuals with T1D could indicate that activated T cells are enabled to unrestrictedly kill the insulin producing beta cells. This is the first study showing absence of galectin-10(hi) eosinophilic subgroup in individuals with T1D compared with healthy controls. This study is a first important step toward unraveling the role of the eosinophils in patients with T1D. |
format | Online Article Text |
id | pubmed-10199897 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-101998972023-05-22 Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes Larsson, Helen Albinsson Högberg, Sofie Lind, Marcus Rabe, Hardis Lingblom, Christine Sci Rep Article Type 1 diabetes (T1D) is an autoimmune disease caused by T-cell mediated destruction of pancreatic beta cells. Eosinophils are found in pancreatic tissue from individuals with T1D. Eosinophilic suppression of T cells is dependent of the protein galectin-10. Little is known when it comes to the role of eosinophil granulocytes in type 1 diabetes. Here we show that individuals with long-standing T1D had lower levels of galectin-10(hi) eosinophils and a subgroup of galectin-10(hi) eosinophils were entirely absent in all T1D patients. In addition, 7% immature eosinophils were present in the circulation of T1D patients whereas 0.8% in healthy individuals. Furthermore, higher levels of CD4+CD8+ T cells and Th17 cells were observed in patients with T1D. Blood samples from 12 adult individuals with long-standing T1D and 12 healthy individuals were compared using cytometry by time-of-flight. Lower levels of galectin-10(hi) eosinophils, which are potent T cell suppressors, in individuals with T1D could indicate that activated T cells are enabled to unrestrictedly kill the insulin producing beta cells. This is the first study showing absence of galectin-10(hi) eosinophilic subgroup in individuals with T1D compared with healthy controls. This study is a first important step toward unraveling the role of the eosinophils in patients with T1D. Nature Publishing Group UK 2023-05-20 /pmc/articles/PMC10199897/ /pubmed/37210405 http://dx.doi.org/10.1038/s41598-023-35300-7 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Larsson, Helen Albinsson Högberg, Sofie Lind, Marcus Rabe, Hardis Lingblom, Christine Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes |
title | Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes |
title_full | Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes |
title_fullStr | Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes |
title_full_unstemmed | Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes |
title_short | Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetes |
title_sort | investigating immune profile by cytof in individuals with long-standing type 1 diabetes |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10199897/ https://www.ncbi.nlm.nih.gov/pubmed/37210405 http://dx.doi.org/10.1038/s41598-023-35300-7 |
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