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C-reactive protein in rheumatology: biology and genetics

Nature Reviews Rheumatology volume 7, pages 282–289 (2011)Cite this article

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Abstract

Measurement of serum C-reactive protein (CRP) level is in widespread clinical use as a sensitive marker of inflammation. CRP has a role in the clearance of bacteria and of dying and altered cells, and might also have more complex immunomodulatory functions. Impaired clearance of apoptotic cells is important in the pathogenesis of systemic lupus erythematosus (SLE), raising the possibility that CRP dysregulation plays a part in this process. We review the available functional and genetic evidence supporting a role for CRP in the pathogenesis of SLE, but recognize that inconsistencies in the existing data mean that conclusions have to be interpreted with caution. More consistent is the evidence that the genetic variants influencing basal CRP level also influence the magnitude of the acute-phase rise in CRP level in active inflammation. Initial reports suggest that these genetic effects might be large enough to directly influence clinical decision-making processes that are based on an interpretation of CRP thresholds. This concept is explored further in this article, particularly in relation to the use of the CRP-based disease activity score in the evaluation of rheumatoid arthritis, where a systematic under-scoring or over-scoring of disease activity could result from a failure to consider the genetic influences on CRP level.

Key Points

  • Serum C-reactive protein (CRP) level is a widely used clinical marker of inflammation, but the underlying pathophysiological role of CRP is less well understood

  • CRP is a key component of the human acute-phase response, coating bacteria and dying cells to facilitate their removal

  • Some biological evidence suggests that CRP has a role in the pathogenesis of systemic lupus erythematosus (SLE), consistent with the 'waste-disposal' hypothesis

  • Although reported in several studies, the association between CRP gene variants and SLE is inconsistent and should be interpreted with caution

  • There is no indication that the blunted CRP response characteristic of active SLE is a genetically-mediated phenomenon

  • CRP gene variants exert a marked influence on the magnitude of the acute-phase CRP response, which could have consequences for the use of CRP in clinical diagnosis and management

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Figure 1: Functional CRP pathways.
Figure 2: Genetics of CRP.

References

  1. Pepys, M. B. & Hirschfield, G. M. C-reactive protein: a critical update. J. Clin. Invest. 111, 1805–1812 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Pereira da Silva, J. A., Elkon, K. B., Hughes, G. R., Dyck, R. F. & Pepys, M. B. C-reactive protein levels in systemic lupus erythematosus: a classification criterion? Arthritis Rheum. 6, 770–771 (1980).

    Article  Google Scholar 

  3. Tillett, W. S. & Francis, T. Serological reactions in pneumonia with non-protein fraction of pneumococcus. J. Exp. Med. 52, 561–571 (1930).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Volanakis, J. E. & Kaplan, M. H. Specificity of C-reactive protein for choline phosphate residues of pneumococcal C-polysaccharide. Proc. Soc. Exp. Biol. Med. 136, 612–614 (1971).

    Article  CAS  PubMed  Google Scholar 

  5. Du Clos, T. W., Zlock, L. T. & Rubin, R. L. Analysis of the binding of C-reactive protein to histones and chromatin. J. Immunol. 141, 4266–4270 (1988).

    CAS  PubMed  Google Scholar 

  6. Du Clos, T. W. C-reactive protein reacts with the U1 small nuclear ribonucleoprotein. J. Immunol. 143, 2553–2559 (1989).

    CAS  PubMed  Google Scholar 

  7. Pepys, M. B., Rowe, I. F. & Baltz, M. L. C-reactive protein: binding to lipids and lipoproteins. Int. Rev. Exp. Pathol. 27, 83–111 (1985).

    CAS  PubMed  Google Scholar 

  8. Hurlimann, J., Thorbecke, G. J. & Hochwald, G. M. The liver as the site of C-reactive protein formation. J. Exp. Med. 123, 365–378 (1966).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Baumann, H. & Gauldie, J. The acute phase response. Immunol. Today 15, 74–80 (1994).

    Article  CAS  PubMed  Google Scholar 

  10. Shine, B., de Beer, F. C. & Pepys, M. B. Solid phase radioimmunoassays for human C-reactive protein. Clin. Chim. Acta 117, 13–23 (1981).

    Article  CAS  PubMed  Google Scholar 

  11. Gabay, C. & Kushner, I. Acute-phase proteins and other systemic responses to inflammation. N. Engl. J. Med. 340, 448–454 (1999).

    Article  CAS  PubMed  Google Scholar 

  12. Choi, Y. S., Hur, J. & Jeong, S. β-catenin binds to the downstream region and regulates the expression C-reactive protein gene. Nucleic Acids Res. 35, 5511–5519 (2007).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Ganter, U., Arcone, R., Toniatti, C., Morrone, G. & Ciliberto, G. Dual control of C-reactive protein gene expression by interleukin-1 and interleukin-6. EMBO J. 8, 3773–3779 (1989).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Kleemann, R. et al. Fibrates down-regulate IL-1-stimulated C-reactive protein gene expression in hepatocytes by reducing nuclear p50-NFκB–C/EBP-β complex formation. Blood 101, 545–551 (2003).

    Article  CAS  PubMed  Google Scholar 

  15. Kushner, I., Samols, D. & Magrey M. A unifying biologic explanation for “high-sensitivity” C-reactive protein and “low-grade” inflammation. Arthritis Care Res. (Hoboken) 62, 442–446 (2010).

    Article  CAS  Google Scholar 

  16. Elliott, P. et al. Genetic loci associated with C-reactive protein levels and risk of coronary heart disease. JAMA 302, 37–48 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  17. Ridker, P. M. et al. Loci related to metabolic-syndrome pathways including LEPR, HNF1A, IL6R, and GCKR associate with plasma C-reactive protein: the Women's Genome Health Study. Am. J. Hum. Genet. 82, 1185–1192 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Mold, C., Gewurz, H. & Du Clos, T. W. Regulation of complement activation by C-reactive protein. Immunopharmacology 42, 23–30 (1999).

    Article  CAS  PubMed  Google Scholar 

  19. Volanakis, J. E. Complement activation by C-reactive protein complexes. Ann. NY Acad. Sci. 389, 235–250 (1982).

    Article  CAS  PubMed  Google Scholar 

  20. Lu, J. et al. Structural recognition and functional activation of FcγR by innate pentraxins. Nature 456, 989–992 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  21. Peisajovich, A., Marnell, L., Mold, C. & Du Clos, T. W. C-reactive protein at the interface between innate immunity and inflammation. Expert Rev. Clin. Immunol. 4, 379–390 (2008).

    Article  CAS  PubMed  Google Scholar 

  22. Gershov, D., Kim, S., Brot, N. & Elkon, K. B. C-reactive protein binds to apoptotic cells, protects the cells from assembly of the terminal complement components, and sustains an antiinflammatory innate immune response: implications for systemic autoimmunity. J. Exp. Med. 192, 1353–1364 (2000).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  23. Sjowall, C. et al. Solid-phase classical complement activation by C-reactive protein (CRP) is inhibited by fluid-phase CRP-C1q interaction. Biochem. Biophys. Res. Commun. 352, 251–258 (2007).

    Article  CAS  PubMed  Google Scholar 

  24. Eisenhardt, S. U., Habersberger, J. & Peter, K. Monomeric C-reactive protein generation on activated platelets: the missing link between inflammation and atherothrombotic risk. Trends Cardiovasc. Med. 19, 232–237 (2009).

    Article  CAS  PubMed  Google Scholar 

  25. Ji, S. R. et al. Monomeric C-reactive protein activates endothelial cells via interaction with lipid raft microdomains. FASEB J. 23, 1806–1816 (2009).

    Article  CAS  PubMed  Google Scholar 

  26. Eisenhardt, S. U., Thiele, J. R., Bannasch, H., Stark, G. B. & Peter, K. C-reactive protein: how conformational changes influence inflammatory properties. Cell Cycle 8, 3885–3892 (2009).

    Article  CAS  PubMed  Google Scholar 

  27. Mihlan, M., Stippa, S., Jozsi, M. & Zipfel, P. F. Monomeric CRP contributes to complement control in fluid phase and on cellular surfaces and increases phagocytosis by recruiting factor H. Cell Death Differ. 16, 1630–1640 (2009).

    Article  CAS  PubMed  Google Scholar 

  28. Casciola-Rosen, L. A., Anhalt, G. & Rosen, A. Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes. J. Exp. Med. 179, 1317–1330 (1994).

    Article  CAS  PubMed  Google Scholar 

  29. Fadok, V. A. et al. Exposure of phosphatidylserine on the surface of apoptotic lymphocytes triggers specific recognition and removal by macrophages. J. Immunol. 148, 2207–2216 (1992).

    CAS  PubMed  Google Scholar 

  30. Kim, S. J., Gershov, D., Ma, X., Brot, N. & Elkon, K. B. I-PLA2 activation during apoptosis promotes the exposure of membrane lysophosphatidylcholine leading to binding by natural immunoglobulin M antibodies and complement activation. J. Exp. Med. 196, 655–665 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Lauber, K. et al. Apoptotic cells induce migration of phagocytes via caspase-3-mediated release of a lipid attraction signal. Cell 113, 717–730 (2003).

    Article  CAS  PubMed  Google Scholar 

  32. Voll, R. E. et al. Immunosuppressive effects of apoptotic cells. Nature 390, 350–351 (1997).

    Article  CAS  PubMed  Google Scholar 

  33. Herrmann, M. et al. Impaired phagocytosis of apoptotic cell material by monocyte-derived macrophages from patients with systemic lupus erythematosus. Arthritis Rheum. 41, 1241–1250 (1998).

    Article  CAS  PubMed  Google Scholar 

  34. Munoz, L. E. et al. Remnants of secondarily necrotic cells fuel inflammation in systemic lupus erythematosus. Arthritis Rheum. 60, 1733–1742 (2009).

    Article  CAS  PubMed  Google Scholar 

  35. Chang, M. K., Binder, C. J., Torzewski, M. & Witztum, J. L. C-reactive protein binds to both oxidized LDL and apoptotic cells through recognition of a common ligand: phosphorylcholine of oxidized phospholipids. Proc. Natl Acad. Sci. USA 99, 13043–13048 (2002).

    Article  CAS  PubMed  Google Scholar 

  36. Bell, S. A., Faust, H., Schmid, A. & Meurer M. Autoantibodies to C-reactive protein (CRP) and other acute-phase proteins in systemic autoimmune diseases. Clin. Exp. Immunol. 113, 327–332 (1998).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Rosenau, B. J. & Schur, P. H. Antibodies to C reactive protein. Ann. Rheum. Dis. 65, 674–676 (2006).

    Article  CAS  PubMed  Google Scholar 

  38. Sjowall, C., Bengtsson, A. A., Sturfelt, G. & Skogh, T. Serum levels of autoantibodies against monomeric C-reactive protein are correlated with disease activity in systemic lupus erythematosus. Arthritis Res. Ther. 6, R87–R94 (2004).

    Article  CAS  PubMed  Google Scholar 

  39. Rodriguez, W. et al. Reversal of ongoing proteinuria in autoimmune mice by treatment with C-reactive protein. Arthritis Rheum. 52, 642–650 (2005).

    Article  CAS  PubMed  Google Scholar 

  40. Rodriguez, W. et al. Prevention and reversal of nephritis in MRL/lpr mice with a single injection of C-reactive protein. Arthritis Rheum. 54, 325–335 (2006).

    Article  CAS  PubMed  Google Scholar 

  41. Szalai, A. J. et al. Delayed lupus onset in (NZB × NZW)F1 mice expressing a human C-reactive protein transgene. Arthritis Rheum. 48, 1602–1611 (2003).

    Article  CAS  PubMed  Google Scholar 

  42. Carlucci, F., Cook, H. T., Garg, A., Pepys, M. B. & Botto, M. Lack of effect of a single injection of human C-reactive protein on murine lupus or nephrotoxic nephritis. Arthritis Rheum. 62, 245–249 (2010).

    Article  CAS  PubMed  Google Scholar 

  43. Saunders, C. L. & Gulliford, M. C. Heritabilities and shared environmental effects were estimated from household clustering in national health survey data. J. Clin. Epidemiol. 59, 1191–1198 (2006).

    Article  PubMed  Google Scholar 

  44. Vickers, M. A. et al. Genotype at a promoter polymorphism of the interleukin-6 gene is associated with baseline levels of plasma C-reactive protein. Cardiovasc. Res. 53, 1029–1034 (2002).

    Article  CAS  PubMed  Google Scholar 

  45. Wessel, J. et al. C-reactive protein, an 'intermediate phenotype' for inflammation: human twin studies reveal heritability, association with blood pressure and the metabolic syndrome, and the influence of common polymorphism at catecholaminergic/β-adrenergic pathway loci. J. Hypertens. 25, 329–343 (2007).

    Article  CAS  PubMed  Google Scholar 

  46. Szalai, A. J., McCrory, M. A., Cooper, G. S., Wu, J. & Kimberly, R. P. Association between baseline levels of C-reactive protein (CRP) and a dinucleotide repeat polymorphism in the intron of the CRP gene. Genes Immun. 3, 14–19 (2002).

    Article  CAS  PubMed  Google Scholar 

  47. Zee, R. Y. & Ridker, P. M. Polymorphism in the human C-reactive protein (CRP) gene, plasma concentrations of CRP, and the risk of future arterial thrombosis. Atherosclerosis 162, 217–219 (2002).

    Article  CAS  PubMed  Google Scholar 

  48. Hage, F. G. & Szalai, A. J. The role of C-reactive protein polymorphisms in inflammation and cardiovascular risk. Curr. Atheroscler. Rep. 11, 124–130 (2009).

    Article  CAS  PubMed  Google Scholar 

  49. Shen, J. & Ordovas, J. M. Impact of genetic and environmental factors on hsCRP concentrations and response to therapeutic agents. Clin. Chem. 55, 256–264 (2009).

    Article  CAS  PubMed  Google Scholar 

  50. Danesh, J. et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N. Engl. J. Med. 350, 1387–1397 (2004).

    Article  CAS  PubMed  Google Scholar 

  51. Danesh, J. & Pepys, M. B. C-reactive protein and coronary disease: is there a causal link? Circulation 120, 2036–2039 (2009).

    Article  PubMed  Google Scholar 

  52. U. S. National Library of Medicine. National Center for Biotechnology Information single nucleotide polymorphism database [online], (2011).

  53. Ridker, P. M. et al. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N. Engl. J. Med. 344, 1959–1965 (2001).

    Article  CAS  PubMed  Google Scholar 

  54. Verzilli, C. et al. Bayesian meta-analysis of genetic association studies with different sets of markers. Am. J. Hum. Genet. 82, 859–872 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Edberg, J. C. et al. Genetic linkage and association of Fcγ receptor IIIA (CD16A) on chromosome 1q23 with human systemic lupus erythematosus. Arthritis Rheum. 46, 2132–2140 (2002).

    Article  CAS  PubMed  Google Scholar 

  56. Moser, K. L. et al. Genome scan of human systemic lupus erythematosus: evidence for linkage on chromosome 1q in African-American pedigrees. Proc. Natl Acad. Sci. USA 95, 14869–14874 (1998).

    Article  CAS  PubMed  Google Scholar 

  57. Cantor, R. M. et al. Systemic lupus erythematosus genome scan: support for linkage at 1q23, 2q33, 16q12–13, and 17q21–23 and novel evidence at 3p24, 10q23–24, 13q32, and 18q22–23. Arthritis Rheum. 50, 3203–3210 (2004).

    Article  CAS  PubMed  Google Scholar 

  58. Russell, A. I. et al. Polymorphism at the C-reactive protein locus influences gene expression and predisposes to systemic lupus erythematosus. Hum. Mol. Genet. 13, 137–147 (2004).

    Article  CAS  PubMed  Google Scholar 

  59. Jonsen, A. et al. Association between SLE nephritis and polymorphic variants of the CRP and FcγRIIIa genes. Rheumatology (Oxford) 46, 1417–1421 (2007).

    Article  CAS  Google Scholar 

  60. Edberg, J. C. et al. Genetic variation in the CRP promoter: association with systemic lupus erythematosus. Hum. Mol. Genet. 17, 1147–1155 (2008).

    Article  CAS  PubMed  Google Scholar 

  61. Szalai, A. J. et al. Single-nucleotide polymorphisms in the C-reactive protein (CRP) gene promoter that affect transcription factor binding, alter transcriptional activity, and associate with differences in baseline serum CRP level. J. Mol. Med. 83, 440–447 (2005).

    Article  CAS  PubMed  Google Scholar 

  62. Shih, P. B. et al. Genetic variation in C-reactive protein (CRP) gene may be associated with risk of systemic lupus erythematosus and CRP concentrations. J. Rheumatol. 35, 2171–2178 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Kim, H. A., Chun, H. Y., Kim, S. H., Park, H. S. & Suh, C. H. C-reactive protein gene polymorphisms in disease susceptibility and clinical manifestations of Korean systemic lupus erythematosus. J. Rheumatol. 36, 2238–2243 (2009).

    Article  CAS  PubMed  Google Scholar 

  64. Graham, R. R. et al. Genetic variants near TNFAIP3 on 6q23 are associated with systemic lupus erythematosus. Nat. Genet. 40, 1059–1061 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  65. Han, J. W. et al. Genome-wide association study in a Chinese Han population identifies nine new susceptibility loci for systemic lupus erythematosus. Nat. Genet. 41, 1234–1237 (2009).

    Article  CAS  PubMed  Google Scholar 

  66. Harley, J. B. et al. Genome-wide association scan in women with systemic lupus erythematosus identifies susceptibility variants in ITGAM, PXK, KIAA1542 and other loci. Nat. Genet. 40, 204–210 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  67. Hom, G. et al. Association of systemic lupus erythematosus with C8orf13–BLK and ITGAM–ITGAX. N. Engl. J. Med. 358, 900–909 (2008).

    Article  CAS  PubMed  Google Scholar 

  68. Yang, W. et al. Genome-wide association study in Asian populations identifies variants in ETS1 and WDFY4 associated with systemic lupus erythematosus. PLoS Genet. 6, e1000841 (2010).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  69. Szalai, A. J. et al. Systemic lupus erythematosus in a multiethnic US Cohort (LUMINA). XXX: association between C-reactive protein (CRP) gene polymorphisms and vascular events. Rheumatology (Oxford) 44, 864–868 (2005).

    Article  CAS  Google Scholar 

  70. Toloza, S. M. et al. Systemic lupus erythematosus in a multiethnic US cohort (LUMINA). XXIII. Baseline predictors of vascular events. Arthritis Rheum. 50, 3947–3957 (2004).

    Article  PubMed  Google Scholar 

  71. Williams, R. C. Jr, Harmon, M. E., Burlingame, R. & Du Clos T. W. Studies of serum C-reactive protein in systemic lupus erythematosus. J. Rheumatol. 32, 454–461 (2005).

    CAS  PubMed  Google Scholar 

  72. Gabay, C. et al. Absence of correlation between interleukin 6 and C-reactive protein blood levels in systemic lupus erythematosus compared with rheumatoid arthritis. J. Rheumatol. 20, 815–821 (1993).

    CAS  PubMed  Google Scholar 

  73. Enocsson, H. et al. Interferon-α mediates suppression of C-reactive protein: explanation for muted C-reactive protein response in lupus flares? Arthritis Rheum. 60, 3755–3760 (2009).

    Article  CAS  PubMed  Google Scholar 

  74. D'Aiuto, F. et al. C-reactive protein (+1444C>T) polymorphism influences CRP response following a moderate inflammatory stimulus. Atherosclerosis 179, 413–417 (2005).

    Article  CAS  PubMed  Google Scholar 

  75. Motoyama, S. et al. C-reactive protein 1059G>C genetic polymorphism influences serum C-reactive protein levels after esophagectomy in patients with thoracic esophageal cancer. J. Am. Coll. Surg. 209, 477–483 (2009).

    Article  PubMed  Google Scholar 

  76. Perry, T. E. et al. C-reactive protein gene variants are associated with postoperative C-reactive protein levels after coronary artery bypass surgery. BMC Med. Genet. 10, 38 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  77. Suk, D. J. et al. Influence of genetic variation in the C-reactive protein gene on the inflammatory response during and after acute coronary ischemia. Ann. Hum. Genet. 70, 705–716 (2006).

    Article  CAS  Google Scholar 

  78. Brull, D. J. et al. Human CRP gene polymorphism influences CRP levels: implications for the prediction and pathogenesis of coronary heart disease. Arterioscler. Thromb. Vasc. Biol. 23, 2063–2069 (2003).

    Article  CAS  PubMed  Google Scholar 

  79. Rhodes, B. et al. A genetic association study of serum acute-phase C-reactive protein levels in rheumatoid arthritis: implications for clinical interpretation. PLoS Med. 7, e1000341 (2010).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  80. Radboud University Nijmegen Medical Center. DAS-score.nl: disease activity score in rheumatoid arthritis [online], (2011).

  81. Fransen, J., Welsing, P. M., de Kuijzer, R. M. & van Riel, P. L. Disease activity scores using C-reactive protein: CRP may replace ESR in the assessment of RA disease activity [abstract THU0138]. Ann. Rheum. Dis. 62 (Suppl. 1), 151 (2003).

    Google Scholar 

  82. Rhodes, B., Wong, A., Navarra, S. V., Villamin, C. & Vyse, T. J. Genetic determinants of basal C-reactive protein expression in Filipino systemic lupus erythematosus families. Genes Immun. 9, 153–160 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  83. Rhodes, B. et al. Fine-mapping the genetic basis of CRP regulation in African Americans: a Bayesian approach. Hum. Genet. 123, 633–642 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  84. Poole, C. D., Conway, P., Reynolds, A. & Currie, C. J. The association between C-reactive protein and the likelihood of progression to joint replacement in people with rheumatoid arthritis: a retrospective observational study. BMC Musculoskelet. Disord. 9, 146 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  85. van der Helm-van Mil, A. et al. A prediction rule for disease outcome in patients with recent-onset undifferentiated arthritis: how to guide individual treatment decisions. Arthritis Rheum. 56, 433–440 (2007).

    Article  PubMed  Google Scholar 

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  1. Divisions of Genetics and Molecular Medicine and Immunology, Infection and Inflammatory Disease, King's College London, 7th Floor Tower Wing, Guy's Hospital Campus, Great Maze Pond, London, SE1 9RT, UK

    Benjamin Rhodes, Barbara G. Fürnrohr & Timothy J. Vyse

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B. Rhodes and B. G. Fürnrohr researched data for the article and contributed equally to writing the article. B. Rhodes and T. Vyse provided substantial contributions to discussions of the content. All authors contributed equally to review and/or editing of the manuscript before submission.

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Correspondence to Timothy J. Vyse.

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Rhodes, B., Fürnrohr, B. & Vyse, T. C-reactive protein in rheumatology: biology and genetics. Nat Rev Rheumatol 7, 282–289 (2011). https://doi.org/10.1038/nrrheum.2011.37

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