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High-Mobility Group Box 1-Induced Complement Activation Causes Sterile Inflammation.

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High-mobility group box 1 (HMGB1) triggers sterile inflammation by activating the complement system independently of antibodies. This finding reveals a new mechanism for HMGB1 in inflammatory diseases.

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Area of Science:

  • Immunology
  • Molecular Biology

Background:

  • High-mobility group box 1 (HMGB1) is a danger-associated molecular pattern molecule involved in inflammation.
  • HMGB1 can augment septic inflammation by binding to bacterial components.

Purpose of the Study:

  • To investigate the role of HMGB1 in mediating complement activation and sterile inflammation.
  • To elucidate the mechanism by which HMGB1 activates the complement system.

Main Methods:

  • In vitro experiments demonstrating HMGB1 binding to C1q and activation of the classical complement pathway.
  • Analysis of complement activation products (C3a, C5b-9) in response to HMGB1.
  • In vivo studies using acetaminophen-induced hepatotoxicity and ischemia-reperfusion injury mouse models.

Main Results:

  • HMGB1 activates the classical complement pathway in an antibody-independent manner via C1q binding.
  • HMGB1 addition leads to C3a and C5b-9 formation in human plasma and on cell membranes.
  • In vivo models showed HMGB1's role in complement activation during sterile inflammation, with effects modulated by C1q deficiency, sRAGE treatment, and HMGB1 neutralization.

Conclusions:

  • HMGB1 actively mediates complement activation, promoting sterile inflammation through the classical pathway.
  • HMGB1 released during cell necrosis or ischemia can exacerbate sterile inflammatory conditions by triggering complement.
  • Targeting HMGB1-complement interactions may offer therapeutic strategies for sterile inflammatory diseases.