About this Journal Submit a Manuscript Table of Contents
Arthritis
Volume 2012 (2012), Article ID 670579, 7 pages
http://dx.doi.org/10.1155/2012/670579
Review Article

Possible Influence of Resistance to Malaria in Clinical Presentation of Rheumatoid Arthritis: Biological Significance of Natural Selection

1Division of Rheumatology, Department of Internal Medicine, Fundación Valle del Lili and ICESI University School of Medicine, Cali, Colombia
2Laboratory of Immunorheumatology, Carrera 98 N. 18-49, Cali, Colombia

Received 6 August 2012; Accepted 21 October 2012

Academic Editor: Masami Takei

Copyright © 2012 Fabio Bonilla-Abadía et al. 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.

Linked References

  1. D. L. Scott, D. P. M. Symmons, B. L. Coulton, and A. J. Popert, “Long-term outcome of treating rheumatoid arthritis: results after 20 years,” The Lancet, vol. 1, no. 8542, pp. 1108–1110, 1987. View at Scopus
  2. M. Lorenzo, “Rheumatoid arthritis,” Foot and Ankle Clinics, vol. 12, no. 3, pp. 525–537, 2007. View at Publisher · View at Google Scholar · View at Scopus
  3. D. L. Scott, F. Wolfe, and T. W. J. Huizinga, “Rheumatoid arthritis,” The Lancet, vol. 376, no. 9746, pp. 1094–1108, 2010. View at Publisher · View at Google Scholar · View at Scopus
  4. J. T. Birch Jr. and S. Bhattacharya, “Emerging trends in diagnosis and treatment of rheumatoid arthritis,” Primary Care, vol. 37, no. 4, pp. 779–792, 2010. View at Publisher · View at Google Scholar · View at Scopus
  5. N. King, C. T. Hittinger, and S. B. Carroll, “Evolution of key cell signaling and adhesion protein families predates animal origins,” Science, vol. 301, no. 5631, pp. 361–363, 2003. View at Publisher · View at Google Scholar · View at Scopus
  6. R. Dawkins, The Greatest Show on Earth, Free Press, New York, NY, USA, 2009.
  7. J. M. Anaya, P. A. Correa, R. D. Mantilla, F. Jimenez, T. Kuffner, and J. M. McNicholl, “Rheumatoid arthritis in African Colombians from Quibdo,” Seminars in Arthritis and Rheumatism, vol. 31, no. 3, pp. 191–198, 2001. View at Publisher · View at Google Scholar · View at Scopus
  8. G. S. Alarcoacuten, “Is rheumatoid arthritis in African descendants from North and South America the same?” Seminars in Arthritis and Rheumatism, vol. 31, no. 3, pp. 143–145, 2001. View at Publisher · View at Google Scholar · View at Scopus
  9. C. A. Cañas and F. Cañas, “The biological significance of evolution in autoimmune phenomena,” Autoimmune Diseases, vol. 2012, Article ID 784315, 12 pages, 2012. View at Publisher · View at Google Scholar
  10. S. A. Tishkoff and S. M. Williams, “Genetic analysis of African populations: human evolution and complex disease,” Nature Reviews Genetics, vol. 3, no. 8, pp. 611–621, 2002. View at Scopus
  11. X. I. Pliakou, F. P. Koutsouka, D. Damigos, K. L. Bourantas, E. C. Briasoulis, and P. V. Voulgari, “Rheumatoid arthritis in patients with hemoglobinopathies,” Rheumatology International, vol. 32, no. 9, pp. 2889–2892, 2012. View at Publisher · View at Google Scholar · View at Scopus
  12. G. Min-Oo and P. Gros, “Erythrocyte variants and the nature of their malaria protective effect,” Cellular Microbiology, vol. 7, no. 6, pp. 753–763, 2005. View at Publisher · View at Google Scholar · View at Scopus
  13. T. G. Smith, K. Ayi, L. Serghides, C. D. Mcallister, and K. C. Kain, “Innate immunity to malaria caused by Plasmodium falciparum,” Clinical and Investigative Medicine, vol. 25, no. 6, pp. 262–272, 2002. View at Scopus
  14. C. López, C. Saravia, A. Gomez, J. Hoebeke, and M. A. Patarroyo, “Mechanisms of genetically-based resistance to malaria,” Gene, vol. 467, no. 1-2, pp. 1–12, 2010. View at Publisher · View at Google Scholar · View at Scopus
  15. A. Driss, J. M. Hibbert, N. O. Wilson, S. A. Iqbal, T. V. Adamkiewicz, and J. K. Stiles, “Genetic polymorphisms linked to susceptibility to malaria,” Malaria Journal, vol. 10, article 271, 2011. View at Publisher · View at Google Scholar · View at Scopus
  16. M. L. Reinagel, M. Gezen, P. J. Ferguson, S. Kuhn, E. N. Martin, and R. P. Taylor, “The primate erythrocyte complement receptor (CR1) as a privileged site: binding of immunoglobulin G to erythrocyte CR1 does not target erythrocytes for phagocytosis,” Blood, vol. 89, no. 3, pp. 1068–1077, 1997. View at Scopus
  17. T. N. Williams, “Red blood cell defects and malaria,” Molecular and Biochemical Parasitology, vol. 149, no. 2, pp. 121–127, 2006. View at Publisher · View at Google Scholar · View at Scopus
  18. V. Thathy, J. M. Moulds, B. Guyah, W. Otieno, and J. A. Stoute, “Complement receptor 1 polymorphisms associated with resistance to severe malaria in Kenya,” Malaria Journal, vol. 4, article 54, 2005. View at Publisher · View at Google Scholar · View at Scopus
  19. E. Nagayasu, M. Ito, M. Akaki et al., “CR1 density polymorphism on erythrocytes of falciparum malaria patients in Thailand,” American Journal of Tropical Medicine and Hygiene, vol. 64, no. 1-2, pp. 1–5, 2001. View at Scopus
  20. J. P. Bayley, T. H. M. Ottenhoff, and C. L. Verweij, “Is there a future for TNF promoter polymorphisms?” Genes and Immunity, vol. 5, no. 5, pp. 315–329, 2004. View at Publisher · View at Google Scholar · View at Scopus
  21. M. Odeh, “The role of tumour necrosis factor-α in the pathogenesis of complicated Falciparum malaria,” Cytokine, vol. 14, no. 1, pp. 11–18, 2001. View at Publisher · View at Google Scholar · View at Scopus
  22. J. C. Knight, I. Udalova, A. V. S. Hill et al., “A polymorphism that affects OCT-1 binding to the TNF promoter region is associated with severe malaria,” Nature Genetics, vol. 22, no. 2, pp. 145–150, 1999. View at Publisher · View at Google Scholar · View at Scopus
  23. D. Kwiatkowski, “Genetic susceptibility to malaria getting complex,” Current Opinion in Genetics and Development, vol. 10, no. 3, pp. 320–324, 2000. View at Publisher · View at Google Scholar · View at Scopus
  24. P. W. Hedrick, “Population genetics of malaria resistance in humans,” Heredity, vol. 107, pp. 283–304, 2011. View at Publisher · View at Google Scholar · View at Scopus
  25. D. P. Kwiatkowski, “How malaria has affected the human genome and what human genetics can teach us about malaria,” American Journal of Human Genetics, vol. 77, no. 2, pp. 171–192, 2005. View at Publisher · View at Google Scholar · View at Scopus
  26. K. Nistala and K. J. Murray, “Co-existent sickle cell disease and juvenile rheumatoid arthritis. Two cases with delayed diagnosis and severe destructive arthropathy,” Journal of Rheumatology, vol. 28, no. 9, pp. 2125–2128, 2001. View at Scopus
  27. M. R. Clatworthy, L. Willcocks, B. Urban et al., “Systemic lupus erythematosus-associated defects in the inhibitory receptor FcγRIIb reduce susceptibility to malaria,” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 17, pp. 7169–7174, 2007. View at Publisher · View at Google Scholar · View at Scopus
  28. V. Khurana and T. P. Bradley, “Adult-onset Still's disease associated with G6PD deficiency: a case report and literature review,” Journal of the Association for Academic Minority Physicians, vol. 9, no. 3, pp. 56–58, 1998. View at Scopus
  29. A. Chatzikyriakidou, P. V. Voulgari, and A. A. Drosos, “What is the role of HLA-B27 in spondyloarthropathies?” Autoimmunity Reviews, vol. 10, no. 8, pp. 464–468, 2011. View at Publisher · View at Google Scholar · View at Scopus
  30. L. M. Gómez, C. Cañas, and J. M. Anaya, “Fcy receptors and autoimmunity,” Acta Médica Colombiana, vol. 30, pp. 27–35, 2005.
  31. C. Kyogoku, H. M. Dijstelbloem, N. Tsuchiya et al., “Fcγ receptor gene polymorphisms in Japanese patients with systemic lupus erythematosus: contribution of FCGR2B to genetic susceptibility,” Arthritis and Rheumatism, vol. 46, no. 5, pp. 1242–1254, 2002. View at Publisher · View at Google Scholar · View at Scopus
  32. U. Siriboonrit, N. Tsuchiya, M. Sirikong et al., “Association of Fcγ receptor IIb and IIIb polymorphisms with susceptibility to systemic lupus erythematosus in Thais,” Tissue Antigens, vol. 61, no. 5, pp. 374–383, 2003. View at Publisher · View at Google Scholar · View at Scopus
  33. M. Waisberg, T. Tarasenko, B. K. Vickers et al., “Genetic susceptibility to systemic lupus erythematosus protects against cerebral malaria in mice,” Proceedings of the National Academy of Sciences of the United States of America, vol. 108, no. 3, pp. 1122–1127, 2011. View at Publisher · View at Google Scholar · View at Scopus
  34. L. C. Willcocks, E. J. Carr, H. A. Niederer et al., “A defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosus,” Proceedings of the National Academy of Sciences of the United States of America, vol. 107, no. 17, pp. 7881–7885, 2010. View at Publisher · View at Google Scholar · View at Scopus
  35. K. G. C. Smith and M. R. Clatworthy, “FcγRIIB in autoimmunity and infection: evolutionary and therapeutic implications,” Nature Reviews Immunology, vol. 10, no. 5, pp. 328–343, 2010. View at Publisher · View at Google Scholar · View at Scopus
  36. T. Tiller, J. Kofer, C. Kreschel et al., “Development of self-reactive germinal center B cells and plasma cells in autoimmune FcγRIIB-deficient mice,” Journal of Experimental Medicine, vol. 207, no. 12, pp. 2767–2778, 2010. View at Publisher · View at Google Scholar · View at Scopus
  37. S. K. Nath, J. B. Harley, and Y. H. Lee, “Polymorphisms of complement receptor 1 and interleukin-10 genes and systemic lupus erythematosus: a meta-analysis,” Human Genetics, vol. 118, no. 2, pp. 225–234, 2005. View at Publisher · View at Google Scholar · View at Scopus
  38. A. Kumar, A. N. Malaviya, S. Sinha, P. S. Khandekar, K. Banerjee, and L. M. Srivastava, “C3b receptor (CR1) genomic polymorphism in rheumatoid arthritis: low receptor levels on erythrocytes are an acquired phenomenon,” Immunologic Research, vol. 13, no. 1, pp. 61–71, 1994. View at Scopus
  39. D. Khanna, H. Wu, G. Park et al., “Association of tumor necrosis factor α polymorphism, but not the shared epitope, with increased radiographic progression in a seropositive rheumatoid arthritis inception cohort,” Arthritis and Rheumatism, vol. 54, no. 4, pp. 1105–1116, 2006. View at Publisher · View at Google Scholar · View at Scopus
  40. Y. H. Lee, Y. H. Rho, S. J. Choi, J. D. Ji, and G. G. Song, “Association of TNF-alpha -308 G/A polymorphism with responsiveness to TNF-α-blockers in rheumatoid arthritis: a meta-analysis,” Rheumatology International, vol. 27, no. 2, pp. 157–161, 2006. View at Publisher · View at Google Scholar · View at Scopus
  41. G. J. Graham, M. Locati, A. Mantovani, A. Rot, and M. Thelen, “The biochemistry and biology of the atypical chemokine receptors,” Immunology Letters, vol. 145, no. 1-2, pp. 30–38, 2012. View at Publisher · View at Google Scholar · View at Scopus
  42. S. Hosaka, T. Akahoshi, C. Wada, and H. Kondo, “Expression of the chemokine superfamily in rheumatoid arthritis,” Clinical and Experimental Immunology, vol. 97, no. 3, pp. 451–457, 1994. View at Scopus
  43. T. Akahoshi, H. Endo, H. Kondo et al., “Essential involvement of interleukin-8 in neutrophil recruitment in rabbits with acute experimental arthritis induced by lipopolysaccharide and interleukin-1,” Lymphokine and Cytokine Research, vol. 13, no. 2, pp. 113–116, 1994. View at Scopus
  44. M. H. Yang, F. X. Wu, C. M. Xie et al., “Expression of CC chemokine ligand 5 in patients with rheumatoid arthritis and its correlation with disease activity and medication,” Chinese Medical Sciences Journal, vol. 24, no. 1, pp. 50–54, 2009. View at Publisher · View at Google Scholar · View at Scopus
  45. M. Norii, M. Yamamura, M. Iwahashi, A. Ueno, J. Yamana, and H. Makino, “Selective recruitment of CXCR3+ and CCR5+ CD4+ T cells into synovial tissue in patients with rheumatoid arthritis,” Acta Medica Okayama, vol. 60, no. 3, pp. 149–157, 2006. View at Scopus
  46. V. Pokorny, F. McQueen, S. Yeoman et al., “Evidence for negative association of the chemokine receptor CCR5 d32 polymorphism with rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 64, no. 3, pp. 487–490, 2005. View at Publisher · View at Google Scholar · View at Scopus
  47. S. K. Lin, H. H. Chang, Y. J. Chen et al., “Epigallocatechin-3-gallate diminishes CCL2 expression in human osteoblastic cells via up-regulation of phosphatidylinositol 3-kinase/Akt/Raf-1 interaction: a potential therapeutic benefit for arthritis,” Arthritis and Rheumatism, vol. 58, no. 10, pp. 3145–3156, 2008. View at Publisher · View at Google Scholar · View at Scopus
  48. D. Smolarek, O. Bertrand, M. Czerwinski, Y. Colin, C. Etchebest, and A. G. de Brevern, “Multiple interests in structural models of DARC transmembrane protein,” Transfusion Clinique et Biologique, vol. 17, no. 3, pp. 184–196, 2010. View at Publisher · View at Google Scholar · View at Scopus
  49. A. M. Patterson, H. Siddall, G. Chamberlain, L. Gardner, and J. Middleton, “Expression of the Duffy antigen/receptor for chemokines (DARC) by the inflamed synovial endothelium,” Journal of Pathology, vol. 197, no. 1, pp. 108–116, 2002. View at Publisher · View at Google Scholar · View at Scopus
  50. E. Smith, H. M. McGettrick, M. A. Stone et al., “Duffy antigen receptor for chemokines and CXCL5 are essential for the recruitment of neutrophils in a multicellular model of rheumatoid arthritis synovium,” Arthritis and Rheumatism, vol. 58, no. 7, pp. 1968–1973, 2008. View at Publisher · View at Google Scholar · View at Scopus
  51. V. Pittoni, S. Vaglio, L. Magrini et al., “Polymorphism of the Duffy erythrocyte chemokine receptor in Italian patients with Behçet's disease,” Rheumatology International, vol. 23, no. 3, pp. 116–120, 2003. View at Scopus
  52. M. K. Mannoor, A. Weerasinghe, R. C. Halder et al., “Resistance to malarial infection is achieved by the cooperation of NK1.1+ and NK1.1- Subsets of intermediate TCR cells which are constituents of innate immunity,” Cellular Immunology, vol. 211, no. 2, pp. 96–104, 2001. View at Publisher · View at Google Scholar · View at Scopus