Host immune and epithelial signaling pathways (None)

Host immune and epithelial signaling pathways represent the complex network of biochemical interactions between the body's barrier-forming epithelial cells and the underlying immune system [1]. These pathways are essential for maintaining tissue homeostasis, coordinating defense against pathogens, and regulating inflammatory responses at mucosal surfaces such as the gut, lungs, and skin [2]. Epithelial cells act as sensors that detect environmental stimuli via pattern recognition receptors and communicate with immune cells through the secretion of cytokines, chemokines, and antimicrobial peptides [3]. Conversely, immune cells produce factors that influence epithelial barrier function, proliferation, and repair mechanisms [1, 4]. Dysregulation of these signaling axes is a hallmark of various inflammatory and autoimmune conditions, including inflammatory bowel disease (IBD), asthma, and psoriasis [1, 2]. While not a single molecular target, specific components within these pathways—such as Janus kinases (JAKs), tumor necrosis factor (TNF), and various interleukins—serve as critical therapeutic targets for modern biologics and small molecules [3, 4]. Therapeutic strategies often aim to restore the balance of these interactions to promote mucosal healing and resolve chronic inflammation [1]. Sources: [1] Nature Reviews Gastroenterology & Hepatology (2019) 16:99-110; [2] Nature Reviews Immunology (2008) 8:193-204; [3] Nature Reviews Immunology (2014) 14:299-312; [4] Frontiers in Immunology (2017) 8:1474.

Other names

Epithelial-immune axisMucosal immune signalingHost-epithelial crosstalkEpithelial-immune interactome

Modulation of cytokine signaling, inhibition of intracellular kinase cascades (e.g., JAK-STAT), and neutralization of inflammatory ligands to restore mucosal barrier integrity and immune homeostasis [1, 3].