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C2 by-pass: Cross-talk between the complement classical and alternative pathways.

A Laich1, H Patel2, A Zarantonello3

  • 1MRC Immunochemistry Unit, Department of Biochemistry, University of Oxford, UK.

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|May 14, 2022
PubMed
Summary
This summary is machine-generated.

Factor B (FB) can substitute for C2 in the complement system, compensating for C2 deficiency. This finding explains why some individuals with C2 deficiency exhibit mild or no systemic lupus erythematosus symptoms.

Keywords:
ComplementHumanImmunodeficiency diseases

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Area of Science:

  • Immunology
  • Complement System Biology
  • Molecular Medicine

Background:

  • Deficiencies in classical complement pathway (CP) components are linked to systemic lupus erythematosus (SLE).
  • However, many individuals with C2 deficiency show mild or no SLE symptoms, suggesting a compensatory mechanism.
  • The alternative pathway (AP) component Factor B (FB) is structurally similar to C2.

Purpose of the Study:

  • To investigate if Factor B (FB) can substitute for C2 in the complement system.
  • To explore the potential compensatory role of FB in C2-deficient individuals.
  • To elucidate the molecular interactions and enzymatic activities involved in this compensation.

Main Methods:

  • Surface Plasmon Resonance (SPR) using BIACORE to assess binding interactions between complement components.
  • Utilized C4b as an immobilized ligand and FB as an analyte.
  • Investigated the cleavage of Factor B by Factor D in the presence of C4b.
  • Assessed the ability of a 'hybrid' C4bBb convertase to cleave and activate C3.

Main Results:

  • Factor B (FB) demonstrated binding to C4b, with an estimated binding constant of 2.00 * 10^-5 M.
  • C2 binding to a C3b-like molecule was not observed.
  • C4b was shown to support the cleavage of FB by Factor D.
  • The C4bBb complex exhibited low but detectable in vitro activity in cleaving and activating C3.

Conclusions:

  • Factor B (FB) can functionally substitute for C2 in the complement system.
  • This FB-mediated compensation mechanism likely explains the mild or absent SLE symptoms in some C2-deficient individuals.
  • The formation of a 'hybrid' C4bBb convertase provides a pathway for C3 activation in the absence of C2.