Danger signals activating innate immunity in graft-versus-host disease.

摘要: Extensive cell death with consecutive release of danger signals can cause immune-mediated tissue destruction. The abundance is likely to determine the relevance as physiological mechanisms that counteract immune activation may be overruled. Such constellation conceivable in chemo-/radiotherapy-induced damage, reperfusion injury, trauma, and severe infection. Studies on graft-versus-host disease (GvHD) development have consider effects chemo-/radiotherapy-related damage leading exogenous endogenous signals. Our previous work has demonstrated a role for adenosine-5′-triphosphate (ATP) an signal GvHD. Besides ATP, uric acid or soluble extracellular matrix components are functional activate NLRP3 inflammasome when released from dying cells matrix. In contrast sterile inflammation, GvHD more complex since bacterial leak through damaged intestinal barriers skin pattern recognition receptors directly contribute pathogenesis. These transmit via toll-like NOD-like innate system. This review covers both impact activating immunity