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. Author manuscript; available in PMC: 2015 Nov 1.
Published in final edited form as: J Immunol. 2014 Sep 22;193(9):4368–4380. doi: 10.4049/jimmunol.1400876

FIGURE 9. Evidence for IFNγ but not IL17 in autoimmune damage to the pancreatic islet caused by CTLA4 down-modulation.

FIGURE 9

(A) Effects of anti-IFNγ antibody treatment on diabetes incidence in juvenile CTLA4RNAi/B6.H2g7 mice. (B) Summary of islet infiltration in anti-IFNγ or control-antibody treated mice (n=4 per group). Each bar represents one animal. (C) Representative H&E stained sections of the pancreas from 6-month-old mice on the B6 genetic background (original magnification: x12.5). (D) Summary of islet infiltration in 6-month-old mice on the B6 genetic background. Control mice were CTLA4RNAi-transgene-negative littermates. (E) Flow cytometry analyses of the TEFF and TEM subsets of the CD4+ Tconv cell compartment in the PLN and pancreas (numbers represent percentages of gated CD4+ Tconv population). (F) Frequencies and total cell numbers of CD4+ TEM subset in IL17+ and IL17– CTLA4RNAi/B6 mice (n=3 per group). Each data-point represents one animal (Mean ± SEM). *p<0.05; ns, not significant.