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- W2314253222 abstract "Type 1 diabetes is a chronic autoimmune disease characterised by the presence of memory autoreactive CD4+ and CD8+ T cells that mediate islet beta cell destruction. We asked whether there are changes in the distributions of major and rare memory T cell subsets in the children with type 1 diabetes. Peripheral blood samples from 47 children at diabetes onset, aged 7 – 11 years, and from 47 age-matched autoantibody negative control children were processed for multi-parameter FACS analysis for markers of memory lymphocytes and the surface markers CD25, CCR7, CXCR5, CCR4, CCR10, CRTH2, CCR6 and CXCR3. Boolean gating was used to quantify major and rare phenotypes. The distribution of CD4+ central memory and effector memory, and CD8+ effector memory and TEMRA cells did not differ between patients and controls. However, several rare populations of CD8+ memory and CD4+ memory were altered in patients. These included increases in a novel CCR10+ CRTH2- Tc22 cell population in both the CD8+ effector memory and TEMRA cells (p < 0.001). This subpopulation of cells yields IL-22 and IL-17 enhanced responses. In contrast, the corresponding CD4+ CCR10+ CRTH2- effector memory phenotype cells were reduced in the blood of patients with type 1 diabetes (p = 0.01), and the resulting CD8/CD4 ratio for this subtype was >three-fold higher in patients (p < 0.001). We suggest that these findings may be explained by an acute expansion of effector CD8+ T cells and recruitment of effector CD4+ T cells to the pancreas around diabetes onset." @default.
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- W2314253222 date "2014-05-06" @default.
- W2314253222 modified "2023-09-27" @default.
- W2314253222 title "Imbalance of rare CCR10+ CD8+ and CD4+ memory T cells in children at onset of type 1 diabetes" @default.
- W2314253222 doi "https://doi.org/10.1055/s-0034-1375048" @default.
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