The role of both naturally occurring CD4+CD25+ Tregs and IL-10-secreting Tregs in infection has been the subject of several recent excellent reviews [9,10]. However, it seems that its response to trauma, burns, hemorrhagic shock, and microbial infection is associated with only a transient proinflammatory period followed by a more prolonged period of immune definitely suppression [11]. Thus, it is speculated that there are some other factors involved in this process.Numerous studies show that an increased burn size leads to higher mortality of burned patients [12,13]. It was also implicated that the extent of burn size might be associated with the development of sepsis.

It is now believed that along with the body’s hyperinflammatory response designated to eliminate the invading pathogen, mechanisms primarily aimed at controlling this initial response are initiated, but may turn out to be deleterious with immune dysfunctions and even death. A similar state of immune suppression has been described after numerous forms of severe trauma [14-16].Although more and more evidence for immune dysfunction after sepsis has been accumulated the mechanisms underlying its development and how it acts to worsen the morbid state of the critically ill patient are yet to be elucidated. In this context, although the majority of clinical and basic researches conducted so far have focused on the roles of myeloid cell populations [17], the contribution of T lymphocytes [18,19] and, in particular, of Tregs has been somewhat ignored. Whether CD4+CD25+ Tregs participate directly in sepsis-induced immunoparalysis resulting in poor outcomes remains to be investigated.

The purpose of the present study was to investigate the significance of changes in activity of Tregs in severely burned patients, and its relation with pathogenesis of sepsis as well as the outcome of the patients following major burns.Materials and methodsParticipants and demographyOne hundred and six patients who were admitted to our burns unit with total burn surface area (TBSA) larger than 30% were included in the present study over a time period of 10 months. Patients were resuscitated according to the Parkland formula using colloid and Ringer’s lactate. Within 48 hours of admission all patients had undergone most burn wound excision for full-thickness burns, and the excision wounds were covered with available autologous skin, and allograft was used to cover any remaining open wounds.

Five to ten days after healing of the donor area, the remaining wounds were totally covered with autograft skin.The thermally injured patients were stratified into three groups according to burn size: 30 to 49% Cilengitide TBSA burns (group I, n = 41), 50 to 69% TBSA burns (group II, n = 34), and more than 70% TBSA burns (group III, n = 31).