title: Pentraxins (CRP, SAP) in the process of complement activation and clearance of apoptotic bodies through Fcγ receptors.
abstract: OBJECTIVE
  Ischemia/reperfusion injury and organ allograft rejection both entail excessive cell and tissue destruction. A number of innate immune proteins, including the pentraxins, participate in the removal of this potentially inflammatory and autoimmunogenic material. The classical pentraxins, C-reactive protein (CRP) and serum amyloid P component (SAP) are serum opsonins, which bind to damaged membranes and nuclear autoantigens. Understanding the role of pentraxins in inflammation has been advanced by the recent identification and structural analysis of their receptor interactions.
  
  
  RESULTS
  The ligand-binding, complement-activating and opsonic properties of pentraxins have been known for some time. However, the establishment of Fcγ receptors as the primary receptors for pentraxins is a recent finding with important implications for CRP and SAP functions. The crystal structure of SAP in complex with FcγRIIa was recently solved, leading to new insights into function and new opportunities for pentraxin-based therapeutics. In addition, new approaches to inhibit CRP synthesis or binding are being developed based on clinical associations between CRP levels and cardiovascular disease.
  
  
  CONCLUSIONS
  This review will summarize data on the function of pentraxins in clearance of injured tissue and cells and discuss the implications of this clearance pathway for autoimmunity and ischemia/reperfusion injury.
authors.affiliation: Department of Veterans Affairs Medical Center and the University of New Mexico School of Medicine, Albuquerque, New Mexico 87108, USA. tduclos@unm.edu
authors.forename: Terry W
authors.initials: TW
authors.lastname: Du Clos
authors.forename: Carolyn
authors.initials: C
authors.lastname: Mold
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology; D002097:C-Reactive Protein / Q000276:immunology* / Q000378:metabolism; D003167:Complement Activation / Q000276:immunology*; D006801:Humans; D007511:Ischemia / Q000276:immunology / Q000473:pathology; D008958:Models, Molecular; D017452:Receptors, IgG / Q000276:immunology* / Q000378:metabolism; D015427:Reperfusion Injury / Q000276:immunology / Q000473:pathology; D000683:Serum Amyloid P-Component / Q000276:immunology* / Q000378:metabolism
chemical_list: D017452:Receptors, IgG; D000683:Serum Amyloid P-Component; D002097:C-Reactive Protein