T-cell-dependent fibrosis in the mdx dystrophic mouse.

摘要: In Duchenne muscular dystrophy patients, the pathological hallmark of disease, namely, chronic accumulation sclerotic scar tissue in interstitial space skeletal muscle is attributed to manifestation secondary processes. Such anomalous generation matrix protein thought be driven by continuous degeneration and regeneration both Muscular Dystrophy mdx mouse homolog. We examined control strain C57bl/10 mice over a range ages with respect amounts collagen present muscles other organs, finding that have significantly higher content at later time points their kidney lung as well muscles. Surprisingly, when we bred on nu/nu background, course fibrogenesis was modified depending different age-matched mice. Transplantation normal thymic into mdx-nu/nu replenished T-cells concomitantly altered tissues levels comparable those immunocompetent This suggests play role onset fibrotic events undermines ability dystrophic regenerate.