• Mayra A Diosa-Toro, Fabián A Jaimes B, María T Rugeles L, and Paula A Velilla H.
• Sede de Investigación Universitaria, Universidad de Antioquia, Medellín, Colombia.
• Rev Chilena Infectol. 2011 Dec 1;28(6):572-8.

AbstractSepsis, defined as a systemic inflammatory response syndrome caused by an infection, is a significant cause of mortality worldwide. It is currently accepted that death associated to sepsis is due to an immune hyperactivation state involving the development of a broad proinflammatory response along with alterations in the coagulation system. It is now clear that besides the inflammatory events, the clinical course of sepsis is characterized by the development of an anti-inflammatory response that could lead to death in its attempt to balance the initial response. The purpose of this review is to summarize current mechanisms that explain the pathogenesis of sepsis, underlying the role that cells with immunoregulatory properties play during the course of this complex syndrome. A better understanding of these processes will contribute in the search of more successful therapeutic strategies.

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