Sepsis remains a leading cause of morbidity and mortality worldwide, with the lung serving both as a frequent site of primary infection and as a pivotal hub for systemic inflammation. In this chapter, we outline the fundamental architecture of pulmonary immunity, detailing the interplay between innate and adaptive defenses—from pathogen-sensing alveolar macrophages, dendritic cells, and neutrophils that orchestrate cytokine cascades to T and B lymphocytes that drive antigen presentation and immunological memory. We also highlight the physical and biochemical barriers in the lung—mucociliary clearance, surfactant proteins, antimicrobial peptides, and the alveolar-capillary interface—as essential first lines of defense. Subsequently, we dissect how the lung immunity is dysregulated in sepsis. An initial hyperinflammatory phase, often culminating in a cytokine storm, gives way to profound immunosuppression. Neutrophil and macrophage dysfunctions exacerbate tissue injury, while endothelial and epithelial dysfunctions drive vascular leakage and acute lung injury. Finally, we briefly summarize pattern-recognition receptor–mediated molecular pathways of immune dysregulation in the lung during sepsis and discuss emerging insights into immunometabolism that reveal how shifts in glucose and lipid pathways further compromise pulmonary immune competence. Together, these sections weave a comprehensive narrative of how sepsis reshapes lung immunity and lay the groundwork for targeted therapies aimed at restoring balance and improving patient outcomes.