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.

Abstract-Infiltration of monocytes into the arterial wall is an early cellular event in atherogenesis. Recent evidence shows that C-reactive protein (CRP) is deposited in the arterial intima at sites of atherogenesis. In this study, we demonstrate that CRP deposition precedes the appearance of monocytes in early atherosclerotic lesions. CRP is chemotactic for freshly isolated human blood monocytes. A specific CRP receptor is demonstrated on monocytes in vitro as well as in vivo, and blockage of the receptor by use of a monoclonal anti-receptor antibody completely abolishes CRP-induced chemotaxis. CRP may play a major role in the recruitment of monocytes during atherogenesis. (Arterioscler Thromb Vasc

A full-length C-reactive protein (CRP) cDNA clone has been isolated from a CBA/J-strain-mouse acute-phase liver library. The 1614-nucleotide cDNA specifies mRNA 5' and 3' untranslated regions of 81 and 858 bases respectively that flank 675 bases encoding mouse pre-CRP. The derived amino acid sequence predicts a 19-residue leader peptide followed by a 206-residue mature mouse CRP that shows considerable sequence identity with both human and rabbit CRP. Northern-blot analysis of mouse liver CRP mRNA concentrations after inflammatory stimuli and comparison with hepatic induction of mRNA for the major mouse acute-phase protein serum amyloid P component established that CRP, a major acute-phase reactant in human and rabbit, is a minor acute-phase reactant in mouse. The size and organization of the mouse CRP mRNA 5' and 3' untranslated regions are significantly different from those of human and rabbit CRP mRNA and may have implications for its anomalous minimal induction during acute inflammation.