Abstract
The study by Souza-Fonseca-Guimaraes and colleagues in the previous issue of Critical Care shows several alterations in blood natural killer (NK) characteristics during human sepsis and systemic inflammatory response syndrome, including changes in NK cell numbers, Toll-like receptor (TLR) expression, and responsiveness to TLR agonists. This paper advances our knowledge of NK cell biology during sepsis and provides the background for future investigations.
Highlights
The study by Souza-Fonseca-Guimaraes and colleagues in the previous issue of Critical Care shows several alterations in blood natural killer (NK) characteristics during human sepsis and systemic inflammatory response syndrome, including changes in NK cell numbers, Toll-like receptor (TLR) expression, and responsiveness to TLR agonists
Impaired interferon gamma (IFNγ) production is considered a hallmark of sepsis-induced immunosuppression [4,5], yet the contribution of NK cell dysfunction to sepsis-induced immunosuppression has not been determined and deserves further consideration
The mechanisms underlying the drop in blood NK cell numbers are not completely clear, but recent studies have documented that NK cells migrate from blood into sites of infection early during the course of sepsis in mice [7,8]
Summary
The study by Souza-Fonseca-Guimaraes and colleagues in the previous issue of Critical Care shows several alterations in blood natural killer (NK) characteristics during human sepsis and systemic inflammatory response syndrome, including changes in NK cell numbers, Toll-like receptor (TLR) expression, and responsiveness to TLR agonists. Medical Center Drive, Nashville, TN 37232, USA This report documents attenuated ex vivo interferon gamma (IFNγ) production by NK cells from patients with sepsis or SIRS in response to TLR agonists and NK cellactivating cytokines. Diminished NK cell function may impair the host response to ongoing and secondary infections.
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