To be, or not to be immunocompetent.
Several data support the view that impairment of the inflammatory-immune response is a hallmark of severe sepsis and the level and time of recovery to immunocompetence has a major impact on the clinical outcome of ICU patients. Recent studies demonstrate that improvement of anti-tumour immune response by targeting negative regulatory molecules, such as CD25, chronic T-lymphocyte activation antigen 4, and programmed death-1 receptor (PD-1)/PD-1 L, offers a novel opportunity to prevent or even reverse progression of tumour growth in experimental models and patients. Likewise, severe sepsis is associated with enhanced expression of those negative regulatory molecules, suggesting a novel approach to reverse immunoparalysis in sepsis. Consequently, targeting negative molecules in sepsis can reverse immunoparalysis and improve survival in experimental sepsis, as shown by Chang and colleagues in a recent issue of Critical Care. This opens new opportunities to overcome overwhelming downregulation of the adaptive immune response to prevent and/or improve recovery from sepsis.
Hans-Dieter
HD
Volk
Petra
P
Reinke
D000818:Animals; D000906:Antibodies / Q000627:therapeutic use*; D060890:B7-H1 Antigen / Q000037:antagonists & inhibitors*; D060908:CTLA-4 Antigen / Q000037:antagonists & inhibitors*; D016469:Fungemia / Q000276:immunology* / Q000628:therapy*; D008297:Male; D061026:Programmed Cell Death 1 Receptor / Q000037:antagonists & inhibitors*
D000906:Antibodies; D060890:B7-H1 Antigen; D060908:CTLA-4 Antigen; D061026:Programmed Cell Death 1 Receptor