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Continual low-level activation of the classical complement pathway.

A P Manderson1, M C Pickering, M Botto

  • 1Division of Immunology and Cell Biology, John Curtin School of Medical Research, The Australian National University, Canberra ACT 2601, Australia.

The Journal of Experimental Medicine
|September 19, 2001
PubMed
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The classical complement pathway can be activated by a "C1-tickover" mechanism, leading to spontaneous C3 activation in plasma. This pathway, requiring C1q, C4, C2, and Ig, amplifies complement activation in vivo.

Area of Science:

  • Immunology
  • Complement System Biology

Background:

  • The classical complement pathway is a key part of the innate immune system.
  • Previous understanding suggested the alternative pathway's C3-tickover as the primary spontaneous activation mechanism.

Purpose of the Study:

  • To investigate and characterize the "C1-tickover" mechanism of classical complement pathway activation.
  • To determine the in vivo relevance of this pathway in humans and mice.

Main Methods:

  • Analysis of freshly collected mouse and human plasma.
  • Utilized complement and immunoglobulin-deficient mouse models.
  • Studied plasma from a human with C1q deficiency before and after C1q infusion.
  • Investigated the effect of blood stasis on complement activation.

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Main Results:

  • Spontaneous C3 activation and C3 fragment generation were observed in fresh plasma.
  • Classical pathway activation required C1q, C4, C2, and plasma Ig, with amplification by the alternative pathway.
  • A similar pathway was confirmed in humans.
  • Elevated C3 levels in deficient mice supported continuous complement activation via both pathways.
  • Blood stasis stimulated classical pathway C3 activation.

Conclusions:

  • The "C1-tickover" is a significant mechanism for antigen-independent classical complement pathway activation.
  • This pathway contributes to continuous complement consumption and may augment immune responses at inflammatory sites.