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In summary, while prolonged UV-A exposure to mice in vivo induces a variety of cataract morphologies that differ to those observed in humans, these studies showed that elevated protein insolubility and impaired enzyme function are caused by UV-B irradiation

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Future therapeutic strategies should pivot from mere receptor blockade to targeting the core upstream drivers of checkpoint expression, such as epigenetic reprogramming, key cytokine signaling, or metabolic dysregulation, to fundamentally reverse the T-cell exhaustion program