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Open Access Rheumatol. 2018 May 25;10:55-60. doi: 10.2147/OARRR.S162512. eCollection 2018.

Serum heat-shock protein-65 antibody levels are elevated but not associated with disease activity in patients with rheumatoid arthritis and ankylosing spondylitis.

Open access rheumatology : research and reviews

Hasan Ulusoy, Gurkan Akgol, Arif Gulkesen, Arzu Kaya, Gul Ayden Kal, Dilara Kaman, Turkan Tuncer

Affiliations

  1. Department of Rheumatology, Medicana International Samsun Hospital, Samsun, Turkey.
  2. Division of Rheumatology, Department of Physical Medicine and Rehabilitation, Firat University, Faculty of Medicine, Elazig, Turkey.
  3. Department of Biochemistry, Firat University, Faculty of Medicine, Elazig, Turkey.

PMID: 29872356 PMCID: PMC5973434 DOI: 10.2147/OARRR.S162512

Abstract

OBJECTIVES: Heat-shock proteins (HSPs) have gained increased interest for their role in autoimmune disorders. These proteins are targeted by the immune system in various autoimmune diseases. The aim of this study was to assess the serum heat-shock protein-65 antibody (anti-HSP65) levels and their clinical significance in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS).

PATIENTS AND METHODS: A total of 30 patients with RA, 30 patients with AS, and 30 healthy controls were enrolled in this study. All patients were assessed using routine clinical and laboratory evaluations. Serum anti-HSP65 levels were determined by ELISA.

RESULTS: Serum anti-HSP65 levels of both RA and AS patients were significantly higher than those of controls (

CONCLUSION: In this study, serum anti-HSP65 levels were increased, but not associated with disease activity in both RA and AS patients. These results suggest that HSP antigens may play a role in the pathogenesis. However, further follow-up studies are needed. Identification of target antigens such as HSP65 is vital to developing new immunotherapeutic agents.

Keywords: HSP; ankylosing spondylitis; heat-shock protein; rheumatoid arthritis

Conflict of interest statement

Disclosure The authors report no conflicts of interest in this work.

References

  1. Arthritis Rheum. 2002 Jul;46(7):1937-46 - PubMed
  2. Autoimmune Dis. 2013;2013:621417 - PubMed
  3. Joint Bone Spine. 2012 Jan;79(1):63-6 - PubMed
  4. Arthritis Rheum. 2004 Feb 15;51(1):14-9 - PubMed
  5. Ann Rheum Dis. 2006 May;65(5):590-4 - PubMed
  6. Semin Arthritis Rheum. 1993 Jun;22(6):357-74 - PubMed
  7. Semin Arthritis Rheum. 2010 Oct;40(2):164-75 - PubMed
  8. Arthritis Rheum. 1984 Apr;27(4):361-8 - PubMed
  9. Autoimmun Rev. 2009 Mar;8(5):388-93 - PubMed
  10. Arthritis Rheum. 2008 Dec;58(12 ):3765-75 - PubMed
  11. Clin Exp Pharmacol Physiol. 2014 Jan;41(1):67-72 - PubMed
  12. BMC Musculoskelet Disord. 2014 Jul 25;15:253 - PubMed
  13. Clin Rheumatol. 1994 Jun;13(2):261-4 - PubMed
  14. Immunol Cell Biol. 1992 Oct;70 ( Pt 5):295-300 - PubMed
  15. Arthritis Rheum. 1998 May;41(5):778-99 - PubMed
  16. Joint Bone Spine. 2009 Dec;76(6):623-8 - PubMed
  17. PLoS One. 2013;8(2):e56210 - PubMed
  18. Ann Rheum Dis. 1993 Jul;52(7):542-4 - PubMed
  19. Arthritis Rheum. 1988 Mar;31(3):315-24 - PubMed
  20. Cell Stress Chaperones. 2008 Summer;13(2):119-25 - PubMed
  21. Lancet. 2001 Nov 24;358(9295):1749-53 - PubMed
  22. Crit Rev Immunol. 2000;20(6):451-69 - PubMed
  23. Semin Arthritis Rheum. 1996 Oct;26(2):558-63 - PubMed
  24. Clin Exp Immunol. 1993 Jun;92(3):404-11 - PubMed
  25. Autoimmunity. 2012 Sep;45(6):449-59 - PubMed
  26. Arthritis Rheum. 2010 Nov;62(11):3221-31 - PubMed
  27. Evid Based Complement Alternat Med. 2011;2011:986797 - PubMed
  28. Proc Natl Acad Sci U S A. 2004 Mar 23;101(12):4228-33 - PubMed
  29. J Rheumatol. 1994 Sep;21(9):1694-8 - PubMed
  30. Arthritis Rheum. 1997 Aug;40(8):1409-19 - PubMed
  31. Scand J Immunol. 1989 Nov;30(5):519-27 - PubMed
  32. Br J Rheumatol. 1990 Dec;29(6):426-9 - PubMed
  33. Nat Rev Immunol. 2007 Jun;7(6):429-42 - PubMed
  34. Lancet. 2006 Sep 2;368(9538):855-63 - PubMed
  35. J Rheumatol. 1994 Dec;21(12):2286-91 - PubMed

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