The anti-inflammatory response dominates after septic shock: association of low monocyte HLA-DR expression and high interleukin-10 concentration

Low monocyte HLA-DR expression as an indicator of immunodepression in very low birth weight infants

“…Studies show that several cytokines may cause or contribute to low HLA-DR (8,18,19). In accordance with the interpretation of reduced HLA-DR expression as a mechanism adaptive to an overwhelming burst of inflammatory stimuli, we found significant negative associations among IL-6, IL-8, and HLA-DR.…”

Monitoring Immune Dysfunctions in the Septic Patient: A New Skin for the Old Ceremony

“…We extended these results by illustrating that IL-10 levels remained higher in nonsurvivors until 15 days after the onset of septic shock in a group of 38 patients (54). In parallel, neither TNF-α nor transforming growth factor (TGF)-β values were able to differentiate survivors from nonsurvivors (54). In addition, we observed that IL-10 was the sole cytokine to correlate with mHLA-DR values.…”

“…In addition, we observed that IL-10 was the sole cytokine to correlate with mHLA-DR values. In particular, high IL-10 concentrations at the beginning of shock were negatively correlated with the nadir of mHLA-DR measurements during the 2 weeks of monitoring (54). Consequently, this initial value of IL-10 may reflect the severity of the forthcoming immunoparalysis.…”

Mechanisms of sepsis‐induced immunosuppression and immunological modification therapies for sepsis

“…In clinical studies, the magnitude and the persistent nature of this refractory state are associated with increased mortality. Two major consequences of endotoxin tolerance on monocytes are an increase in the release of immunosuppressive mediators, such as IL‐10, and a decrease in antigen presentation as a result of the reduced expression of human leukocyte antigen (HLA)‐DR; both are associated with a worse outcome of sepsis 20, 21. The continued release of IL‐10 might contribute to sepsis‐induced immunosuppression and thus might augment the susceptibility to secondary microbial infections 22.…”