We thank Ye et al. (1) for pointing out an error that occurred in the production of our article (2). In the final version of the manuscript that was accepted for publication by Diabetes, Fig. 8D showed that the addition of recombinant human interleukin-10 (rhIL-10) with human peripheral blood mononuclear cells (PBMCs) in NOD-SCID IL-2rγ−/− (NSG) mouse recipients of neonatal porcine islet cell cluster (NICC) grafts resulted in reduced interferon-γ (IFN-γ) and enhanced FoxP3, cytotoxic T-cell antigen-4 (CTLA-4), glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR), and IL-10 gene expression when compared with mice receiving human PBMCs alone (2). The results for mice receiving PBMCs and those receiving PBMCs and rhIL-10 should be reversed. The actual data in the figure is correct. The correct and original Fig. 8D is shown below. The wording in the legend text remains unchanged and there has been no change in the results or conclusions—namely, that human regulatory T cells (Tregs) were able to suppress anti-xenograft T-cell effector cell responses and this effect was dependent on IL-10. An erratum to correct the online version of the article is published in this issue of Diabetes.
Real-time PCR analysis of intragraft mRNA expression of Treg function-associated molecules and effector cytokine IFN-γ in neonatal porcine islet cell cluster grafts. Data are presented as mean ± SD of three individual samples from one of two independent experiments. *P < 0.05 compared with PBMC only.
Real-time PCR analysis of intragraft mRNA expression of Treg function-associated molecules and effector cytokine IFN-γ in neonatal porcine islet cell cluster grafts. Data are presented as mean ± SD of three individual samples from one of two independent experiments. *P < 0.05 compared with PBMC only.
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Duality of Interest. No potential conflicts of interest relevant to this article were reported.
