Variable frequencies of peripheral T-lymphocyte subsets in the diabetes spectrum from type 1 diabetes through latent autoimmune diabetes in adults (LADA) to type 2 diabetes
T lymphocytes are key players in the pathogenesis of autoimmune diabetes. We recruited subjects with T1D (n=81), LADA (n=82), T2D (n=95) and NGT (n=218) and analyzed the percentages of T-lymphocyte subsets, including T helper 1 (Th1), T helper 2 (Th2), T helper 17 (Th17), T cytotoxic 1 (Tc1), regula...
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Published in | Frontiers in immunology Vol. 13; p. 974864 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Frontiers Media S.A
24.08.2022
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Subjects | |
Online Access | Get full text |
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Summary: | T lymphocytes are key players in the pathogenesis of autoimmune diabetes. We recruited subjects with T1D (n=81), LADA (n=82), T2D (n=95) and NGT (n=218) and analyzed the percentages of T-lymphocyte subsets, including T helper 1 (Th1), T helper 2 (Th2), T helper 17 (Th17), T cytotoxic 1 (Tc1), regulatory T cells (Tregs), effector T (Teff), naïve T, central memory T (Tcm), and effector memory T (Tem) cells by flow cytometry. LADA patients possessed similar frequencies of IFN-γ
+
CD4
+
T (Th1), IFN-γ
+
CD8
+
T and CD4
+
Teff cells compared with T1D patients, but much lower than those of NGT subjects. Like T2D patients, LADA patients had increased frequencies of CD4
+
Tem and CD8
+
Tem cells with respect to T1D and NGT subjects. In LADA patients, Th2 cells were decreased while CD4
+
Tcm cells were increased compared with NGT subjects. Notably, we observed significant negative correlations between the CD4
+
Tcm cell frequency and C-peptide in LADA subjects. These data demonstrates that LADA patients possess T-cell subset changes resembling both T1D and T2D and represent the middle of the diabetes spectrum between T1D and T2D. Based on these T-cell subset alterations, we speculate that autoimmunity-induced β-cell destruction and inflammation-induced insulin resistance might both be involved in the pathogenesis of LADA. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Agnieszka Paradowska-Gorycka, National Institute of Geriatrics, Rheumatology and Rehabilitation, Poland These authors have contributed equally to this work and share first authorship This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology Reviewed by: Karen Cerosaletti, Benaroya Research Institute, United States; Jon D. Piganelli, University of Pittsburgh, United States |
ISSN: | 1664-3224 1664-3224 |
DOI: | 10.3389/fimmu.2022.974864 |