Investigating immune profile by CyTOF in individuals with long-standing type 1 diabetesShow others and affiliations
2023 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 13, no 1, article id 8171Article in journal (Refereed) Published
Abstract [en]
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-10hi eosinophils and a subgroup of galectin-10hi 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-10hi 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-10hi 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.
Place, publisher, year, edition, pages
Nature Research , 2023. Vol. 13, no 1, article id 8171
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:ri:diva-64928DOI: 10.1038/s41598-023-35300-7Scopus ID: 2-s2.0-85160403348OAI: oai:DiVA.org:ri-64928DiVA, id: diva2:1766092
Note
Funding details: VGFOUFBD-964924; Funding details: Åke Wiberg Stiftelse, M21-0125; Funding details: Magnus Bergvalls Stiftelse, 2022-02812; Funding details: Centre for Antibiotic Resistance Research, University of Gothenburg, CARe; Funding text 1: Open access funding provided by University of Gothenburg. This study was funded by grants from the Magnus Bergvalls foundation (2022-02812), Åke Wibergs foundation (M21-0125), Wilhelm and Martina Lundgrens Science foundation and the Fyrbodal Research and Development Council Region Västra Götaland (identification number VGFOUFBD-964924).
2023-06-122023-06-122024-02-12Bibliographically approved