Host immune signaling at the gut interface

Host immune signaling at the gut interface refers to the complex regulatory network of interactions between the intestinal microbiota, the epithelial barrier, and the underlying mucosal immune system (Mowat & Agace, 2014). This process is not a single therapeutic target but rather a physiological environment where multiple signaling pathways, including those mediated by pattern recognition receptors (PRRs) and various cytokines, maintain homeostasis or drive inflammation (Belkaid & Hand, 2014). In diseases like inflammatory bowel disease (IBD), this signaling becomes dysregulated, leading to chronic inflammation and tissue damage (Xavier & Podolsky, 2007). Therapeutic strategies often target specific components of this interface, such as tumor necrosis factor (TNF), interleukins (IL-12/23), or integrins, to restore balance and promote mucosal healing (Neurath, 2017). Understanding these interactions is crucial for developing precision medicines that can modulate the gut-immune axis without compromising systemic immunity (Danese et al., 2015).

Other names

Mucosal immune signalingGut-immune axisIntestinal immune homeostasisHost-microbe crosstalkGastrointestinal immune signaling

Modulation of specific cytokine pathways (e.g., TNF-alpha or IL-23 inhibition) or blockade of leukocyte trafficking (e.g., alpha-4-beta-7 integrin antagonism) to restore mucosal homeostasis (Neurath, 2017).