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- W4313373562 abstract "Abstract Background IL-2 is a well characterized cytokine that drives the expansion of activated human T cells. Its mechanism of action involving the high affinity receptor CD25 confers to IL-2 a crucial role in the homeostasis and function of regulatory T cell (Treg) basally expressing CD25. It has been suggested that low doses of IL-2 treatment in vivo, selectively expands Tregs without altering effector T cell or NK populations. This preferential targeting is key to cell-based immunotherapeutics that aim to prevent autoimmunity such as Type 1 Diabetes. Methods A phase I protocol was initiated to treat recently diagnosed T1D patients with a single infusion of ex-vivo expanded autologous polyclonal Tregs followed by two 5-days courses of low-dose IL-2. Patients were monitored for safety and diabetes-related metabolic profiles. PBMCs were analyzed at different time points by CyToF and 10X genomic single-cell RNAseq to monitor T cell activation. Results The overall safety profile was excellent but all 9 patients treated with the combined therapy failed to maintain c-peptide production at pre-treatment levels. We observed an expansion of Tregs and granzyme B (GZMB)+ NK subsets. More interestingly, single cell T cell receptor and gene expression sequencing allowed us to detected in all the patients a population of (GZMB)-producing CD8+ T that expanded clonally after IL-2 treatment. Conclusion These data suggest that the usage of low-dose IL-2 together with polyclonal Tregs infusion exacerbate the expansion of Tregs but also of a GZMB+ CD8+ T cells and NK population already present in blood. Thus, the failure for all patients to maintain C-peptide level may be due to a shift of the immune balance toward activation rather than tolerance." @default.
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- W4313373562 date "2020-05-01" @default.
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- W4313373562 title "Effect of combined low dose IL-2 and polyclonal Tregs infusion in Type 1 Diabetes patients" @default.
- W4313373562 doi "https://doi.org/10.4049/jimmunol.204.supp.224.49" @default.
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