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Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
Published on: June 15, 2019
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Sepsis in PD-1 light.
Guillaume Monneret1,2, Morgane Gossez3,4, Fabienne Venet3,4
1Hospices Civils de Lyon, Immunology Laboratory, Hôpital E. Herriot, 5, place d'Arsonval, 69437, Lyon, Cedex, 03, France. guillaume.monneret@chu-lyon.fr.
Critical Care (London, England)
|July 6, 2016
Summary
Sepsis causes immune suppression, leading to T-cell exhaustion. Blocking immune checkpoints like PD-1 may offer new treatments for septic shock patients, potentially improving survival rates.
Area of Science:
- Immunology
- Critical Care Medicine
- Oncology
Background:
- Sepsis induces profound immunosuppression after initial inflammation.
- Immune cell exhaustion, similar to cancer, is a key feature.
- Co-inhibitory receptors play a role in sepsis-induced immune dysfunction.
Purpose of the Study:
- To explore the role of co-inhibitory receptors in lymphocyte exhaustion during sepsis.
- To investigate programmed cell death protein 1 (PD-1) expression as a predictor of mortality in septic shock.
Main Methods:
- Reviewing mechanisms of sepsis-induced immune alterations.
- Analyzing the expression of PD-1 on lymphocytes and PD-L1 on monocytes in septic shock patients.
- Correlating PD-1/PD-L1 expression with patient mortality.
Main Results:
- Sepsis leads to significant immunosuppression and T-cell exhaustion.
- PD-1 expression on lymphocytes and PD-L1 on monocytes are linked to sepsis severity.
- Elevated PD-1/PD-L1 expression may predict mortality in septic shock.
Conclusions:
- Lymphocyte exhaustion via co-inhibitory receptors is a critical aspect of sepsis.
- PD-1 pathway modulation presents a potential therapeutic target for sepsis.
- PD-1 expression can serve as a prognostic biomarker in septic shock.

