Figure 1.

Features of innate immune deficiency in advanced cirrhosis. Host and microbial inflammatory mediators resulting from liver injury and gut bacterial translocation initially activate innate immune cells, contributing to inflammation and the development, and progression of liver cirrhosis. Chronic stimulation progressively perturbs innate immune sensing and surveillance functions, contributing to infection risk in patients with decompensated cirrhosis. Genetic and environmental factors also contribute to immune dysfunction. The features of cellular and humoral innate immune deficiency commonly identified in cohorts of patients with advanced cirrhosis are summarized. DAMP, Damage Associated Molecular Pattern; PAMP, Pathogen Associated Molecular Pattern; PRR, Pattern Recognition Receptor; PPI, Proton Pump Inhibitor; MBL, Mannose Binding Lectin; TLR, Toll-like receptor.