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Our study has conclusively demonstrated that cigarette smoke exposure has a profound suppressive effect on the generation of adaptive immune responses to NTHI and suggests the mechanism by which prior cigarette smoke exposure predisposes chronic obstructive pulmonary disease patients to recurrent infections, leading to exacerbations and contributing to mortality

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In response to cumulative cellular stresses such as telomere attrition, oxidative stress, DNA damage, and mitochondrial dysfunction, proliferative cells activate canonical pathways, including the p53p21 and p16 INK4A -RB axes, which enforce durable growth arrest

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