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 inFrontiers in immunology Vol. 13; p. 974864
Main Authors Tan, Tingting, Xiang, Yufei, Deng, Chao, Cao, Chuqing, Ren, Zhihui, Huang, Gan, Zhou, Zhiguang
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 24.08.2022
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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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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