Abstract
C-reactive protein (CRP) is well-known as a sensitive albeit unspecific biomarker of inflammation. In most rheumatic conditions, the level of this evolutionarily highly conserved pattern recognition molecule conveys reliable information regarding the degree of ongoing inflammation, driven mainly by interleukin-6. However, the underlying causes of increased CRP levels are numerous, including both infections and malignancies. In addition, low to moderate increases in CRP predict subsequent cardiovascular events, often occurring years later, in patients with angina and in healthy individuals. However, autoimmune diseases characterized by the Type I interferon gene signature (e.g., systemic lupus erythematosus, primary Sjögren’s syndrome and inflammatory myopathies) represent exceptions to the general rule that the concentrations of CRP correlate with the extent and severity of inflammation. In fact, adequate levels of CRP can be beneficial in autoimmune conditions, in that they contribute to efficient clearance of cell remnants and immune complexes through complement activation/modulation, opsonization and phagocytosis. Furthermore, emerging data indicate that CRP constitutes an autoantigen in systemic lupus erythematosus. At the same time, the increased risks of cardiovascular and cerebrovascular diseases in patients diagnosed with systemic lupus erythematosus and rheumatoid arthritis are well-established, with significant impacts on quality of life, accrual of organ damage, and premature mortality. This review describes CRP-mediated biological effects and the regulation of CRP release in relation to aspects of cardiovascular disease and mechanisms of autoimmunity, with particular focus on systemic lupus erythematosus.
Highlights
More than 90 years have passed since the discovery of C-reactive protein (CRP) at The Rockefeller University, our current understanding of CRP is essentially based on the original observations made by William S
Autoimmune diseases characterized by the Type I interferon gene signature represent exceptions to the general rule that the concentrations of CRP correlate with the extent and severity of inflammation
Adequate levels of CRP can be beneficial in autoimmune conditions, in that they contribute to efficient clearance of cell remnants and immune complexes through complement activation/modulation, opsonization and phagocytosis
Summary
More than 90 years have passed since the discovery of C-reactive protein (CRP) at The Rockefeller University, our current understanding of CRP is essentially based on the original observations made by William S. They found that sera obtained from patients during the acute phase of pneumococcal pneumonia precipitated with the C-polysaccharide derived from the cell wall of the pneumococcus, and that this reaction diminished as the patients recovered [1,2]. This previously unknown C-reactive substance was later found to be a protein, and was named “C-reactive protein” [1,2]. The integrity of the native pentameric structure of CRP (pCRP) is dependent upon the presence of calcium ions This structure is disrupted irreversibly into monomers under denaturing conditions, e.g., in an acidic microenvironment. This review summarizes recent discoveries related to CRP-mediated biological effects, as well as to the regulation of CRP release with respect to aspects of CVD and mechanisms of autoimmunity
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