The dark side of C5a in sepsis
Ward PA2004Nature reviews. ImmunologyReview
CardiovascularImmune/Innate
Lyme & Co-Infections
Abstract
Sepsis is a major clinical problem for which therapeutic interventions have been largely unsuccessful, in spite of promising strategies that were successful in animals, especially rodents. There is new evidence that sepsis causes excessive activation of the complement system and that this induces paralysis of innate immune functions in phagocytic cells due to effects of the powerful complement-activation product, C5a. This review describes our present understanding of how and why sepsis is a life-threatening condition and how it might be more effectively treated.
Key Biomarkers
C5aMMP9
Symptom Clusters
Complement system activationPhagocytic cell dysfunctionSepsis
Cited By (9)
- The role of complement in danger sensing and transmissionImmunologic Research · 2006
- Harmful molecular mechanisms in sepsisNature reviews. Immunology · 2008
- Complement amplification revisitedMolecular Immunology · 2006
- The role of complement, C5a and its receptors in sepsis and multiorgan dysfunction syndromeJournal of Investigative Surgery · 2006
- THE PRIMING EFFECT OF C5A ON MONOCYTES IS PREDOMINANTLY MEDIATED BY THE P38 MAPK PATHWAYShock · 2007
- Complement-related molecular events in sepsis leading to heart failureMolecular Immunology · 2007
- Hypothesis: combined inhibition of complement and CD14 as treatment regimen to attenuate the inflammatory responseAdvances in experimental medicine and biology · 2008
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