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. 2007 Aug 16;104(34):13756–13761. doi: 10.1073/pnas.0706509104

Fig. 3.

Fig. 3.

Molecular mapping of the CD28 binding motif(s) required for disease induction in CTLA-4-deficient mice. (A) Microscopic views (×100) of pancreatic sections from 4-week-old mice of the indicated strains. (B) Microscopic views (×100) of pancreatic sections of 4-week-old mice from CTLA-4-deficient mice expressing transgenic CD28 molecules. (C) Macroscopic examination of the abdomen of CTLA-4-deficient mice expressing transgenic CD28 molecules. Muscle wasting, absence of pancreas, and accumulation in the gut of undigested food are evident in CTLA-4-deficient mice expressing CD28 molecules with an intact Lck binding motif (CD28-WT, CD28–170, and CD28-NP), whereas no pathology is detected in CTLA-4-deficient mice expressing CD28 molecules without an intact Lck binding motif (CD28-CP, CD28-NCP, and CD28-TL). (D and E) Size and weight comparison of 4-week-old CD28−/−CTLA-4−/− mice expressing transgenic CD28 molecules. Displayed in the bar graph are the mean weight (± SEM) of no less than five mice from each transgenic line. Statistical analysis was by the two-tailed Student t test. NS, not significant (P < 0.02). (F) Survival of CTLA-4-deficient mice expressing transgenic CD28 molecules. Twenty to 30 mice of each transgenic line were observed daily (Left), and their median survival times were determined (Right). Mice alive at day 150 were also alive on day 300.