<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>C-reactive protein (CRP) is a blood component comprised of five identical
            subunits with a combined molecular mass of 110 kDa; in the presence of Ca<sup>++</sup>
            it binds phosphocholine (PC) with high affinity. Ligand-bound CRP activates
            complement and the protein reportedly binds various Fc receptors. Coincident
            with a now decade-long resurgence in clinical interest in associations of CRP with
            disease, our laboratory has been investigating the biology of CRP <italic>in vivo</italic> using
            human CRP transgenic mice (CRPtg). At that time we confirmed that CRP affects
            a host defense function mediated at least in part through the elimination of
            pathogens. Less appreciated and not as well understood as CRP's ability to bind
            antigen and aid in the elimination of microbes, is its known ability to bind
            autoantigens and presumed capacity to promote clearance of apoptotic cells. These
            latter properties of CRP have long been suspected to contribute to homeostasis and
            to autoimmune disease. In this article we review and update the evidence
            generated in CRPtg by our group and <italic>in vitro</italic> by others' that indicates CRP is more
            than just an antimicrobial molecule and convenient marker of inflammation - rather,
            it protects against autoimmunity. A mechanistic
            hypothesis is presented to account for this cause-and-effect relationship.</p>
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Clin Dev Immunol. 2004 Sep-Dec; 11(3-4):221-226