ReviewFrontiers in immunology2026
A crosstalk between the immune system and obstructive sleep apnea.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
4 authors.
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Abstract
Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction during sleep. Its hallmark pathophysiological features, intermittent hypoxia (IH) and sleep fragmentation (SF), trigger cellular and molecular responses that disrupt immune homeostasis. Recurrent hypoxia-reoxygenation promotes oxidative stress and activates hypoxia-inducible factor-1α (HIF-1α), nuclear factor-κB (NF-κB), and the NLRP3 inflammasome, contributing to sustained inflammatory signaling, endothelial dysfunction, and alterations in circulating and tissue-resident immune cells. This review integrates evidence from clinical and preclinical studies linking OSA to dysregulation of innate, adaptive, and humoral immunity and examines how these immune alterations contribute to OSA-associated systemic morbidity. Innate immune dysregulation in OSA is characterized by activation of neutrophils and monocytes/macrophages, increased oxidative stress, and elevated pro-inflammatory mediators, including IL-1β, IL-6, IL-8, TNF-α, CRP, and MCP-1. Altered expressions of ICAM-1 and VCAM-1 may further promote leukocyte recruitment and endothelial dysfunction, sustaining systemic inflammation and end-organ injury. Adaptive immune dysregulation includes alterations in CD4
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