Figure 6
Figure 6. Immunopathology related to TERT-based ACT: tissue histology. (A) Both mTERT-specific (top) and β-gal–specific (bottom) CTL-treated mice did not show any morphologic alteration of liver, kidney, small and large intestine, testis, lungs, and heart as assessed by histologic analysis. Liver sections from treated and control mice showed typical polygonal arrangement of lobules. Portal triads were regularly distributed; neither portal nor centrolobular degeneration was present. Renal specimens of both experimental groups showed normal renal cortex. There were no evidence of glomerular hypercellularity or an increase in thickness of capillary walls, nor was there flogosis or fibrosis of tubulointerstitial compartment. Small (ileum) and large (colon) intestine sections appeared normal: there was no damage of the villous architecture or glandular distortion, and there were no flogistic or fibrotic alterations of the lamina propria. In the testis of mTERT-specific CTL-treated and control-treated mice, seminiferous tubules were normal in size and number; there were no alterations of spermatogenic cell maturation. Healthy lung parenchyma from mTERT-specific CTL-treated and control groups was composed by flat walled alveoli with interposed thin layer of connective tissue and normal bronchial tree. No pathologic alterations were found in heart: normal myocardium composed of striated muscle fibers is shown. (B) Spleen of mTERT-specific CTL-treated mice showed impaired architecture respect to control samples: B-cell rich outer compartment of periarteriolar lymphoid sheets (parentheses, BZ) had a reduced thickness of both follicular (FZ) and marginal zones (dashed lines, MZ). T-cell inner zone (solid lines, TZ) was normal in both groups.

Immunopathology related to TERT-based ACT: tissue histology. (A) Both mTERT-specific (top) and β-gal–specific (bottom) CTL-treated mice did not show any morphologic alteration of liver, kidney, small and large intestine, testis, lungs, and heart as assessed by histologic analysis. Liver sections from treated and control mice showed typical polygonal arrangement of lobules. Portal triads were regularly distributed; neither portal nor centrolobular degeneration was present. Renal specimens of both experimental groups showed normal renal cortex. There were no evidence of glomerular hypercellularity or an increase in thickness of capillary walls, nor was there flogosis or fibrosis of tubulointerstitial compartment. Small (ileum) and large (colon) intestine sections appeared normal: there was no damage of the villous architecture or glandular distortion, and there were no flogistic or fibrotic alterations of the lamina propria. In the testis of mTERT-specific CTL-treated and control-treated mice, seminiferous tubules were normal in size and number; there were no alterations of spermatogenic cell maturation. Healthy lung parenchyma from mTERT-specific CTL-treated and control groups was composed by flat walled alveoli with interposed thin layer of connective tissue and normal bronchial tree. No pathologic alterations were found in heart: normal myocardium composed of striated muscle fibers is shown. (B) Spleen of mTERT-specific CTL-treated mice showed impaired architecture respect to control samples: B-cell rich outer compartment of periarteriolar lymphoid sheets (parentheses, BZ) had a reduced thickness of both follicular (FZ) and marginal zones (dashed lines, MZ). T-cell inner zone (solid lines, TZ) was normal in both groups.

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