Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 126, Issue 1, Pages 23-31Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI82224
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Funding
- American Association for the Surgery of Trauma
- NIH [GM-29507, GM-61656]
- Godfrey D. Stobbe Endowment
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM029507, R37GM029507, R01GM061656] Funding Source: NIH RePORTER
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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.
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