Sepsis-induced immune dysfunction

can immune therapies reduce mortality?

Delano, Matthew J.
Ward, Peter A.

¹Department of Surgery, Division of Acute Care Surgery, University of Michigan, Ann Arbor, Michigan, USA.
²Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan, USA.

Address correspondence to: Peter A. Ward, Godfrey D. Stobbe Professor of Pathology, University of Michigan Medical School, Department of Pathology, 7520 MSRB I, 1301 Catherine Rd., Ann Arbor, Michigan 48109-5602, USA. Phone: 734.647.2921; E-mail: [email protected].

Journal of Clinical Investigation 126(1):p 23-31, January 4, 2016. | DOI: 10.1172/JCI82224

Sepsis is a systemic inflammatory response induced by an infection, leading to organ dysfunction and mortality. Historically, sepsis-induced organ dysfunction and lethality were attributed to the interplay between inflammatory and antiinflammatory responses. With advances in intensive care management and goal-directed interventions, early sepsis mortality has diminished, only to surge later after “recovery” from acute events, prompting a search for sepsis-induced alterations in immune function. Sepsis is well known to alter innate and adaptive immune responses for sustained periods after clinical “recovery,” with immunosuppression being a prominent example of such alterations. Recent studies have centered on immune-modulatory therapy. These efforts are focused on defining and reversing the persistent immune cell dysfunction that is associated with mortality long after the acute events of sepsis have resolved.