Inflammation and Immunity in Radiation Damage to the Gut Mucosa

Figure 2

Radiation exposure to the gut mucosa induces epithelial stem cells apoptosis and clonogenic cell death, endothelial cells death and activation, and mucosal barrier breakdown. Innate immunity: resident immune cells such as macrophages and mast cells are activated by DAMPs generated by dead cells and PAMPs coming from mucosal breakdown. Activated endothelial cells express adhesion molecules and cytokines favouring immune cells recruitment into the injured tissue. Activated macrophages increase neutrophil recruitment, which in turn emit signals favouring monocytes recruitment from the blood stream. The radiation-induced tissue M1/M2 balance is unknown. Adaptative immunity: Th1 lymphocytes can activate innate immune cells and favour cell-mediated immunity, whereas Th2 favour humoral immunity via B cells. The balance in irradiated gut tissue is in favour of a Th2 orientation. Treg maintain immune tolerance. Resident and recruited dendritic cells are activated and carry out the link with lymph nodes and the establishment of specific immune response. PAMPs are also detected by TLRs, whose activation can protect epithelium against radiation damage. ILCs play a role in epithelial homeostasis, but their role after radiation exposure is unknown.