High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.

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High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. (A) Flow cytometric analysis of a range of surface markers on islet-specific P14 CD8+ T cells visualized as a heat map [based on arbitrary intensity units (MFI)]. Significant differences were found in CD69, KLRG1, and PD-1. (B and C) The expression of the activation marker CD69 on Ag-specific P14 CTLs was higher in the group receiving low amounts of non–islet-specific CD8+ T cells. (D and E) The exhaustion marker PD-1 was found to be highly expressed in the HI scenario (D), quantified in (E). Results are representative of two to three independent experiments. Data are means ± SEM. *P < 0.05, two-tailed unpaired Mann-Whitney U tests. (F to J) Islet-specific P14 CTLs isolated from pancreatic draining lymph nodes were stimulated in vitro with their cognate Ag GP33–41 and revealed less effector cytokine production (IFN-γ) [(F) and (G)] and increased IL-10 production [(H) and (I)] in mice receiving HI amounts of non–islet-specific TCR-tg CD8+ T cells; this is quantified in (J). *P < 0.05, two-tailed unpaired Mann-Whitney U tests. FSC, forward scatter. Gustaf Christoffersson et al. Sci. Immunol. 2018;3:eaam6533 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works