The relationship between CD4+CD25+CD127- regulatory T cells and inflammatory response and outcome during shock states.
BACKGROUND
Although regulatory T lymphocytes (Tregs) have a pivotal role in preventing autoimmune diseases and limiting chronic inflammatory conditions, they may also block beneficial immune responses by preventing sterilizing immunity to certain pathogens.


METHODS
To determine whether naturally occurring Treg cells have a role in inflammatory response and outcome during shock state we conducted an observational study in two adult ICUs from a university hospital. Within 12 hours of admission, peripheral whole blood was collected for the measurement of cytokines and determination of lymphocyte count. Sampling was repeated at day three, five and seven. Furthermore, an experimental septic shock was induced in adult Balb/c mice through caecal ligation and puncture.


RESULTS
Forty-three patients suffering from shock (26 septic, 17 non septic), and 7 healthy volunteers were included. The percentage of Tregs increased as early as 3 days after the onset of shock, while their absolute number remained lower than in healthy volunteers. A similar pattern of Tregs kinetics was found in infected and non infected patients. Though there was an inverse correlation between severity scores and Tregs percentage, the time course of Tregs was similar between survivors and non survivors. No relation between Tregs and cytokine concentration was found. In septic mice, although there was a rapid increase in Treg cells subset among splenocytes, antibody-induced depletion of Tregs before the onset of sepsis did not alter survival.


CONCLUSIONS
These data argue against a determinant role of Tregs in inflammatory response and outcome during shock states.
Service de réanimation médicale, Hôpital Central, CHU de Nancy, 29 Bld du Mal de Lattre de Tassigny, Nancy, 54000, France. f.hein@chu-nancy.fr
François
F
Hein
Frédéric
F
Massin
Aurélie
A
Cravoisy-Popovic
Damien
D
Barraud
Bruno
B
Levy
Pierre-Edouard
PE
Bollaert
Sébastien
S
Gibot
D000368:Aged; D000818:Animals; D015704:CD4 Antigens / Q000276:immunology*; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D053645:Interleukin-2 Receptor alpha Subunit / Q000276:immunology*; D053699:Interleukin-7 Receptor alpha Subunit / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008875:Middle Aged; D012772:Shock, Septic / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D015704:CD4 Antigens; D016207:Cytokines; D053645:Interleukin-2 Receptor alpha Subunit; D053699:Interleukin-7 Receptor alpha Subunit