Figure 1

Loss of NK cell activity has no influence on DBA/2J iris disease. Despite some variability from eye to eye, the range and prevalence of phenotypes at each age was indistinguishable between genotypes. The top two panels are representative eyes of B6.D2-Tyrp1^bGpnmb^R150XPrf1^+/+ mice (A-H) at the indicated ages, and the bottom two panels of eyes of B6.D2-Tyrp1^bGpnmb^R150XPrf1^-/- mice (I-P). The top rows of each panel shows broad beam illumination to assess the presence of dispersed pigment within the anterior chamber and iris stromal morphology (A-D and I-L). The bottom rows of each panel shows transillumination (E-H and M-P). This assays the degree of iris depigmentation, detectable as areas within the image where reflected light passes through the iris. The onset and progression of iris disease in the perforin mutants are similar to that in wild-type mice: eyes of young perforin mutant mice have healthy irides (I,M). At 6 mo, mutant mice exhibit mild iris disease characterized by swelling of the peripupillary region (J). At 9 mo, the peripupillary region becomes atrophic, transillumination is prominent (K,O). At 12 mo, there is an increasing degree of iris atrophy including distinct iris holes, profound transillumination and pigment dispersion (L,P).