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. Author manuscript; available in PMC: 2010 Dec 8.
Published in final edited form as: Immunity. 2009 Oct 8;31(4):654–664. doi: 10.1016/j.immuni.2009.08.023

Fig. 2. T cell activation and proliferation in the pancreatic lesion.

Fig. 2

(A–D) Affymetrix M430 2.0 chip data. CD4 T cells were isolated from pancreas lesion and PLN at three different time-points: 0, 15 and 24 hours after DT treatment from BDC2.5/NOD.Foxp3DTR+ mice. (A) Expression versus expression values are plotted for pancreas and PLN at 24 and 15 hours. Numbers indicate count of genes that were more than 2-fold differential expressed. (B–D) Fold-change to fold-change plot. (B) 24 hours versus 0 hour for PLN and pancreas (left panel) and 15 hours versus 0 hour for PLN and pancreas (right panel). Red line in (left panel) represents the linear regression curve. (C) Genes changes after 24 hours (and presented in Supplementary Table S1) are highlighted in the 15 hours versus 0 hour PLN vs. pancreas plot (left panel) and random date control (right panel). (D) Activation/proliferation responsive genes (Hill et al., 2007) over-expressed (red) or under-represented (blue) are highlighted in 24 hours versus 0 hour for PLN and pancreas (left panel) and 15 hours versus 0 hour for PLN and pancreas (right panel). (E) CD4 T cells were stained for early activation marker CD69 at different time-points after DT from pancreas and PLN, from BDC2.5/NOD.Foxp3DTR+ (filled symbols) and BDC2.5/NOD.Foxp3DTR− control mice (open symbols). (F) BrdU staining of CD4 T effector cells: BrdU was injected 48 hours after DT and mice were analyzed after one hour. Pancreas and PLN from BDC2.5/NOD.Foxp3DTR+ or DTR negative control mice were stained for BrdU and CD4. Left panel shows representative dot plots, right panel summarized 4–5 mice from independent experiments with mean and SD, * indicates significant difference (p<0.05).