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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Characterization of the Complement Cascade in Human Traumatic Brain Injury.

Claudia Ann Smith1, Adam Safwat2, Romit Samanta2

  • 1Department of Clinical Neurosciences, University of Cambridge, Cambridge, United Kingdom.

Journal of Neurotrauma
|February 17, 2026
PubMed
Summary
This summary is machine-generated.

This study reveals altered complement protein levels in traumatic brain injury (TBI) patients, with C5 elevation linked to poor outcomes. Further research could explore complement as a TBI therapeutic target.

Keywords:
complementinflammationpatient outcomesecondary injurytraumatic brain injury

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Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Neuroinflammation, driven by complement activation, worsens outcomes in severe traumatic brain injury (TBI).
  • Previous studies on complement in TBI were limited to animal models and post-mortem tissues.
  • Characterizing the complement cascade in a substantial human TBI cohort is crucial.

Purpose of the Study:

  • To investigate the complement cascade, focusing on lectin pathway initiators, in TBI patients versus healthy controls.
  • To analyze temporal profiles of complement proteins post-TBI.
  • To assess the association between complement proteins and clinical outcomes in TBI.

Main Methods:

  • Plasma samples from 64 TBI patients (days 1-7, 42, 365) and 17 controls were analyzed for 10 complement proteins.
  • Proteins included initiators (MBL, MASP2, ficolin3), effectors (C4b, C2, factor D, factor I), and downstream components (C5, C5a, C5b9).
  • Assays used were single and multiplexing protein assays; clinical data included injury severity and Glasgow Outcome Scale Extended.

Main Results:

  • Seven of ten complement proteins differed significantly between TBI patients and controls (p < 0.05).
  • Ficolin3 was significantly lower in TBI patients, persisting even one year post-injury (p < 0.001).
  • Elevated C4b, C5, and factor I were associated with unfavorable outcomes; C5 showed a robust independent prognostic value (OR: 1.53, p < 0.001).

Conclusions:

  • The study characterized the complement cascade in human TBI with high temporal resolution.
  • Complement component C5 is a significant independent predictor of unfavorable outcome 6 months post-TBI.
  • Targeting the complement system presents a potential therapeutic avenue for TBI management.