Ablation of C3 modulates macrophage reactivity in the outer retina during photo-oxidative damage.

摘要: Purpose Dysregulation of the complement cascade contributes to a variety retinal dystrophies, including age-related macular degeneration (AMD). The central component complement, C3, is expressed in abundance by macrophages outer retina, and its ablation suppresses photoreceptor death experimental photo-oxidative damage. Whether this also influences macrophage reactivity model system, however, unknown. We investigate effect C3 on activity phagocytosis during Methods Age-matched knockout (KO) mice wild-type (WT) C57/Bl6 were subjected Measurements nuclear layer (ONL) thickness terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining used assess pathology apoptosis, respectively. Macrophage assessed with immunolabeling for pan-macrophage phagocytic markers, conjunction TUNEL cohorts KO WT mice. Results exhibited protection against cell following damage, which was associated reduction immunoreactivity stress-related factor GFAP. In conjunction, there IBA1-positive retina compared decrease number CD68-positive cells subretinal space. addition, engulfment TUNEL-positive -negative photoreceptors significantly lower cohort damage cohort. Conclusions results show that absence mitigates net impact depletion neuroprotective context These data improve our understanding inhibition inflammation inform development treatments targeting activation diseases such as AMD.