C-reactive protein, inflammation, and innate immunity

Immunol Res. 2001;24(2):163-76. doi: 10.1385/IR:24:2:163.

Abstract

The circulating acute phase reactant C-reactive protein (CRP) has traditionally been characterized as an effector of nonclonal host resistance since it activates the classical complement cascade and mediates phagocytosis, but it is also capable of regulating inflammation. The three-dimensional structure of human CRP has revealed the molecular basis for complement activation and binding of phosphate monoesters. CRP gene expression by liver hepatocytes in response to cytokines (IL-1beta and IL-6) released in tissues requires several transcription factors which interact. Elevated levels of CRP are a prognostic marker for coronary artery disease; however, the role of CRP in atheriosclerosis remains unknown. CRP also mediates direct host protection to some microbial pathogens via its opsonic activity through certain Fcgamma-receptors. The CRP response may be one of the links between nonspecific innate immunity and specific clonal immunity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • C-Reactive Protein / chemistry
  • C-Reactive Protein / immunology*
  • Complement Activation
  • Coronary Artery Disease / immunology
  • Immunity, Innate
  • Inflammation
  • Models, Molecular
  • Phagocytosis
  • Receptors, Immunologic

Substances

  • CRP protein, human
  • Receptors, Immunologic
  • C-Reactive Protein