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Human C-reactive protein: expression, structure, and function.

J E Volanakis1

  • 1Biomedical Sciences Research Center Alexander Fleming, P.O. Box 74145, 166 02 Varkiza, Greece. j.volanakis@fleming.gr

Molecular Immunology
|September 5, 2001
PubMed
Summary
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C-reactive protein (CRP) is a key acute-phase protein that binds phosphocholine on pathogens and damaged cells. It initiates complement and acts as an opsonin, primarily serving as a first line of innate host defense.

Area of Science:

  • Biochemistry
  • Immunology
  • Molecular Biology

Background:

  • C-reactive protein (CRP) is a pentameric acute-phase protein.
  • Interleukin-6 (IL-6) is the primary inducer of CRP gene expression during the acute phase.
  • CRP exhibits Ca-binding specificity for phosphocholine (PCh).

Purpose of the Study:

  • To elucidate the structure and function of C-reactive protein (CRP).
  • To understand CRP's role in host defense mechanisms.
  • To investigate CRP's interactions with pathogens and host cells.

Main Methods:

  • X-ray crystallography was used to determine the crystal structure of CRP.
  • Ligand-binding site analysis was performed.
  • Functional assays investigated CRP's role in complement activation and opsonization.

Related Experiment Videos

  • Transgenic mouse models were utilized to study CRP's in vivo functions.

    • Main Results:

    • The crystal structure revealed the topology and composition of CRP's ligand-binding site.
    • CRP binds to phosphocholine on pathogens and damaged host cells.
    • CRP initiates complement activation via the classical pathway, acting as an opsonin.
    • CRP-mediated complement activation does not promote acute inflammation or membrane damage.
    • Transgenic mice demonstrated protection against bacterial infection and endotoxemia.

    Conclusions:

    • CRP functions as a crucial component of the innate immune system.
    • Its primary roles include bacterial pathogen defense and clearance of apoptotic/necrotic cells.
    • CRP contributes to host defense without mediating detrimental inflammatory responses.