• Fabienne Venet, Chun-Shiang Chung, Hakim Kherouf, Anne Geeraert, Chistophe Malcus, Françoise Poitevin, Julien Bohé, Alain Lepape, Alfred Ayala, and Guillaume Monneret.
• Division of Surgical Research, Rhode Island Hospital, Brown University, Providence, RI, USA.
• Intensive Care Med. 2009 Apr 1; 35 (4): 678-86.

PurposeSepsis syndrome represents the leading cause of death in intensive care unit. Patients present features consistent with a decline in immune responsiveness potentially contributing to mortality. We investigated whether CD4(+)CD25(+) regulatory T cells (Treg) participate in the induction of lymphocyte anergy after sepsis.MethodObservational study in septic shock patients and experimental study in mice.ResultsWe took advantage of the recently described flow cytometric gating strategy using the measurement of CD25 and CD127 expressions for monitoring Treg (CD4(+)CD25(+)CD127(-)Foxp3(+)). In patients the increased circulating Treg percentage significantly correlated with a decreased lympho-proliferative response. In a murine model of sepsis mimicking these observations, the ex vivo downregulation of Foxp3 expression using siRNA was associated with a restoration of this response.ConclusionThe relative increase in circulating Treg might play a role in lymphocyte anergy described after septic shock and represent a standardizable surrogate marker of declining proliferative capacity after sepsis.

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