Fig. 2
Interactions of the innate and adaptive immune systems in response to trauma. Immediately following injury, damaged tissues release damage-associated molecular patterns (DAMPs) and in response, residing innate immune cells release pro-inflammatory cytokines. These signals help recruit other innate immune cells to the site of injury in an attempt to contain the deleterious effects of the injury. However, in severe injuries, the immune response goes beyond the local site of injury and leads to systemic inflammation. To reduce the impact of systemic inflammation, the adaptive immune system, primarily through the suppression of regulatory T cells (Treg), releases anti-inflammatory cytokines and other signals that impede the immune system as it tries to continue the pro-inflammatory response. This manifests as apoptosis of innate immune cells and decreased antigen presentation (HLA-DR on monocytes), as well as apoptosis and the anergy of helper T cells causing leukopenia. In the maladaptive state, preponderance of this anti-inflammatory, immune suppressing phenotype leads to the consequences of CARS and PICS. The general effect of a chronic inflammatory state on immune systems in response to injury is listed below their respective cell types. For a general review of the immune system and inflammation, the reader is referred to a review by Spiering [37]