Table of Contents Author Guidelines Submit a Manuscript
Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 295081, 8 pages
http://dx.doi.org/10.1155/2012/295081
Research Article

Enhanced HMGB1 Expression May Contribute to Th17 Cells Activation in Rheumatoid Arthritis

1Department of Immunology, Institute of Laboratory Medicine, Jiangsu University, Xuefu Road 301, Zhenjiang 212013, China
2Suzhou Municipal Hospital, Suzhou 215002, China
3The Affiliated People's Hospital of Jiangsu University, Zhenjiang 212002, China

Received 3 May 2011; Revised 5 July 2011; Accepted 8 July 2011

Academic Editor: Zoltan Szekanecz

Copyright © 2012 Yan Shi 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. J. S. Smolen, D. Aletaha, J. W. Bijlsma et al., “Treating rheumatoid arthritis to target: recommendations of an international task force,” Annals of the Rheumatic Diseases, vol. 69, no. 4, pp. 631–637, 2010. View at Publisher · View at Google Scholar · View at Scopus
  2. D. A. Von, J. Locke, J. H. Robinson, and W. F. Ng, “Response of Th17 cells to a citrullinated arthritogenic aggrecan peptide in patients with rheumatoid arthritis,” Arthritis and Rheumatism, vol. 62, no. 1, pp. 143–149, 2010. View at Publisher · View at Google Scholar · View at Scopus
  3. W. B. van den Berg and P. Miossec, “IL-17 as a future therapeutic target for rheumatoid arthritis,” Nature Reviews Rheumatology, vol. 5, no. 10, pp. 549–553, 2009. View at Publisher · View at Google Scholar · View at Scopus
  4. U. Andersson and H. Erlandsson-Harris, “HMGB1 is a potent trigger of arthritis,” Journal of Internal Medicine, vol. 255, no. 3, pp. 344–350, 2004. View at Publisher · View at Google Scholar · View at Scopus
  5. R. E. Voll, V. Urbonaviciute, M. Herrmann et al., “High mobility group box 1 in the pathogenesis of inflammatory and autoimmune diseases,” The Israel Medical Association Journal, vol. 10, pp. 26–28, 2008. View at Google Scholar
  6. T. Li, X. Zuo, Y. J. Zhou et al., “The vagus nerve and nicotinic receptors involve inhibition of HMGB1 release and early pro-inflammatory cytokines function in collagen-induced arthritis,” Journal of Clinical Immunology, vol. 30, no. 2, pp. 213–220, 2010. View at Publisher · View at Google Scholar · View at Scopus
  7. H. S. Hreggvidsdottir, T. Östberg, H. Wähämaa et al., “The alarmin HMGB1 acts in synergy with endogenous and exogenous danger signals to promote inflammation,” Journal of Leukocyte Biology, vol. 86, no. 3, pp. 655–662, 2009. View at Publisher · View at Google Scholar · View at Scopus
  8. R. S. Goldstein, A. Bruchfeld, L. Yang et al., “Cholinergic anti-inflammatory pathway activity and high mobility group Box-1 (HMGB1) serum levels in patients with rheumatoid arthritis,” Molecular Medicine, vol. 13, no. 3-4, pp. 210–215, 2007. View at Publisher · View at Google Scholar · View at Scopus
  9. N. Taniguchi, K. Kawahara, K. Yone et al., “High mobility group box chromosomal protein 1 plays a role in the pathogenesis of rheumatoid arthritis as a novel cytokine,” Arthritis and Rheumatism, vol. 48, no. 4, pp. 971–981, 2003. View at Publisher · View at Google Scholar · View at Scopus
  10. R. Kokkola, E. Sundberg, A. K. Ulfgren et al., “High mobility group box chromosomal protein 1: a novel proinflammatory mediator in synovitis,” Arthritis and Rheumatism, vol. 46, no. 10, pp. 2598–2603, 2002. View at Publisher · View at Google Scholar · View at Scopus
  11. R. Pullerits, I. M. Jonsson, M. Verdrengh et al., “High mobility group box chromosomal protein 1, a DNA binding cytokine, induces arthritis,” Arthritis and Rheumatism, vol. 48, no. 6, pp. 1693–1700, 2003. View at Publisher · View at Google Scholar · View at Scopus
  12. S. Muller, P. Scaffidi, B. Degryse et al., “New EMBO members' review: the double life of HMGB1 chromatin protein: architectural factor and extracellular signal,” The EMBO Journal, vol. 20, pp. 4337–4340, 2001. View at Google Scholar
  13. P. Scaffidi, T. Misteli, and M. E. Bianchi, “Release of chromatin protein HMGB1 by necrotic cells triggers inflammation,” Nature, vol. 418, no. 6894, pp. 191–195, 2002. View at Publisher · View at Google Scholar · View at Scopus
  14. C. W. Bell, W. Jiang, C. F. Reich, and D. S. Pisetsky, “The extracellular release of HMGB1 during apoptotic cell death,” American Journal of Physiology, vol. 291, no. 6, pp. C1318–C1325, 2006. View at Publisher · View at Google Scholar · View at Scopus
  15. S. Gardella, C. Andrei, D. Ferrera et al., “The nuclear protein HMGB1 is secreted by monocytes via a non-classical, vesicle-mediated secretory pathway,” EMBO Reports, vol. 3, no. 10, pp. 995–1001, 2002. View at Publisher · View at Google Scholar · View at Scopus
  16. R. Pullerits, M. Bokarewa, I. M. Jonsson, M. Verdrengh, and A. Tarkowski, “Extracellular cytochrome c, a mitochondrial apoptosis-related protein, induces arthritis,” Rheumatology, vol. 44, no. 1, pp. 32–39, 2005. View at Publisher · View at Google Scholar · View at Scopus
  17. F. C. Arnett, S. M. Edworthy, D. A. Bloch et al., “The American rheumatism sssociation 1987 revised criteria for the classification of rheumatoid arthritis,” Arthritis and Rheumatism, vol. 31, no. 3, pp. 315–324, 1988. View at Google Scholar · View at Scopus
  18. Y. Yuan, H. Shen, D. S. Franklin, D. T. Scadden, and T. Cheng, “In vivo self-renewing divisions of haematopoietic stem cells are increased in the absence of the early G1-phase inhibitor, p18INK4C,” Nature Cell Biology, vol. 6, no. 5, pp. 436–442, 2004. View at Publisher · View at Google Scholar · View at Scopus
  19. U. Andersson, H. Wang, K. Palmblad et al., “High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes,” Journal of Experimental Medicine, vol. 192, no. 4, pp. 565–570, 2000. View at Publisher · View at Google Scholar · View at Scopus
  20. H. Park, Z. Li, X. O. Yang et al., “A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17,” Nature Immunology, vol. 6, no. 11, pp. 1133–1141, 2005. View at Publisher · View at Google Scholar · View at Scopus
  21. Y. Chen, C. L. Langrish, B. Mckenzie et al., “Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis,” Journal of Clinical Investigation, vol. 116, no. 5, pp. 1317–1326, 2006. View at Publisher · View at Google Scholar · View at Scopus
  22. Y. Shi, H. Wang, Z. Su et al., “Differentiation imbalance of Th1/Th17 in peripheral blood mononuclear cells might contribute to pathogenesis of Hashimoto's thyroiditis,” Scandinavian Journal of Immunology, vol. 72, no. 3, pp. 250–255, 2010. View at Publisher · View at Google Scholar · View at Scopus
  23. S. Y. Wang, M. Yang, X. Xu et al., “Intranasal delivery of T-bet modulates the profile of helper T cell immune responses in experimental asthma,” Journal of Investigational Allergology and Clinical Immunology, vol. 18, no. 5, pp. 357–365, 2008. View at Google Scholar
  24. E. Lubberts, “Th17 cytokines and arthritis,” Seminars in Immunopathology, vol. 32, no. 1, pp. 43–53, 2010. View at Publisher · View at Google Scholar · View at Scopus
  25. K. Hirota, M. Hashimoto, H. Yoshitomi et al., “T cell self-reactivity forms a cytokine milieu for spontaneous development of IL-17+ Th cells that cause autoimmune arthritis,” Journal of Experimental Medicine, vol. 204, no. 1, pp. 41–47, 2007. View at Publisher · View at Google Scholar · View at Scopus
  26. L. Jens, K. Birgit, J. J. Wang, A. V. Villarino, and A. K. Abbas, “Role of IL-17 and regulatory T lymphocytes in a systemic autoimmune disease,” Journal of Experimental Medicine, vol. 203, no. 13, pp. 2785–2791, 2006. View at Publisher · View at Google Scholar · View at Scopus
  27. Y. Liu, Y. Yuan, Y. Li et al., “Interacting neuroendocrine and innate and acquired immune pathways regulate neutrophil mobilization from bone marrow following hemorrhagic shock,” Journal of Immunology, vol. 182, no. 1, pp. 572–580, 2009. View at Google Scholar · View at Scopus
  28. H. Philippa, J. L. Maggie, and P. Edward, “Investigating the role of the interleukin-23/-17A axis in rheumatoid arthritis,” BowmanRheumatology, vol. 48, no. 12, pp. 1581–1589, 2009. View at Publisher · View at Google Scholar · View at Scopus
  29. M. Penzo, R. Molteni, T. Suda et al., “Inhibitor of NF-κB kinases α and β are both essential for high mobility group box 1-mediated chemotaxis,” Journal of Immunology, vol. 184, no. 8, pp. 4497–4509, 2010. View at Publisher · View at Google Scholar · View at Scopus
  30. J. Li, H. Xie, T. Wen, H. Liu, W. Zhu, and X. Chen, “Expression of high mobility group box chromosomal protein 1 and its modulating effects on downstream cytokines in systemic lupus erythematosus,” Journal of Rheumatology, vol. 37, no. 4, pp. 766–775, 2010. View at Publisher · View at Google Scholar · View at Scopus
  31. V. Urbonaviciute, B. G. Fürnrohr, S. Meister et al., “Induction of inflammatory and immune responses by HMGB1-nucleosome complexes: implications for the pathogenesis of SLE,” Journal of Experimental Medicine, vol. 205, no. 13, pp. 3007–3018, 2008. View at Publisher · View at Google Scholar · View at Scopus
  32. L. Duan, C. Y. Wang, J. Chen et al., “High-mobility group box 1 promotes early acute allograft rejection by enhancing IL-6-dependent Th17 alloreactive response,” Laboratory Investigation, vol. 91, no. 1, pp. 43–53, 2011. View at Publisher · View at Google Scholar · View at Scopus
  33. Z. L. Su, C. X. Sun, C. L. Zhou et al., “HMGB 1 blockade attenuates experimental autoimmune myocarditis possibly by suppressing Th17-cell expansion,” European Journal of Immunology. In press. View at Publisher · View at Google Scholar