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Clinical Rheumatology

, Volume 33, Issue 4, pp 523–529 | Cite as

Clinical parameter and Th17 related to lymphocytes infiltrating degree of labial salivary gland in primary Sjögren’s syndrome

  • Yunyun Fei
  • Wen Zhang
  • Dongfang Lin
  • Chen Wu
  • Mengtao Li
  • Yan Zhao
  • Xiaofeng Zeng
  • Fengchun Zhang
Original Article

Abstract

The aim of this study is to investigate the correlation between clinical parameter, Th17, and degree of lymphocytes infiltrating in labial salivary gland in primary Sjögren’s syndrome (pSS). Minor labial gland biopsies from a cohort of 103 patients fulfilling the American-European consensus classification criteria for pSS were examined and grouped into G1 to G3 according to infiltration degree of lymphocytes in labial salivary glands and formation of germinal center. IL-17 level and Th17 proportion of peripheral blood samples in 54 patients with pSS were analyzed simultaneously. Among the 103 labial salivary glands samples, there were 10.5 % of G1, 68.4 % of G2, and 21.1 % of G3, respectively. Some clinical parameters were markedly associated with the degree of inflammatory cells infiltration in labial glands, including white blood cell counts, lymphocytes, liver enzymes, and pulmonary function diffusion rates. The average optical density of IL-17 correlated with the severity of lymphocytic infiltration in the labial glands, while the proportion of Th17 cells in the peripheral blood mononuclear cells showed no significant relationship to the degree of lymphocytic infiltration in the labial glands from the SS patients. IL-17A mRNA levels in peripheral blood mononuclear cells from pSS patients before immunosuppressant treatment were significantly higher than that in patients after immunosuppressant treatment. The degree of inflammatory cells infiltration in labial glands was related to some clinical manifestations in pSS. IL-17 may play a role in the pathogenesis of lymphocytic infiltration in the labial glands. Immunosuppressive treatment might affect Th17 cells.

Keywords

IL-17 Labial salivary gland Lymphocytes infiltrating Primary Sjögren’s syndrome 

Notes

Funding

This work was supported by the National Natural Science Foundation of China (no. 81202360, 81172858, 81373190), Beijing Natural Science Foundation (7132206).

Disclosures

None.

References

  1. 1.
    Price EJ, Venables PJ (1995) The etiopathogenesis of Sjogren’s syndrome. Semin Arthritis Rheum 25:117–133PubMedCrossRefGoogle Scholar
  2. 2.
    Katsifis GE, Moutsopoulos NM, Wahl SM (2007) T lymphocytes in Sjögren’s syndrome: contributors to and regulators of pathophysiology. Clin Rev Allergy Immunol 32:252–264PubMedCrossRefGoogle Scholar
  3. 3.
    Maehara T, Moriyama M, Hayashida JN et al (2012) Selective localization of T helper subsets in labial salivary glands from primary Sjögren’s syndrome patients. Clin Exp Immunol 169(2):89–99PubMedCentralPubMedCrossRefGoogle Scholar
  4. 4.
    Reksten TR, Jonsson MV, Szyszko EA et al (2009) Cytokine and autoantibody profiling related to histopathological features in primary Sjogren’s syndrome. Rheumatology (Oxford) 48(9):1102–1106CrossRefGoogle Scholar
  5. 5.
    Moriyama M, Hayashida JN, Toyoshima T et al (2012) Cytokine/chemokine profiles contribute to understanding the pathogenesis and diagnosis of primary Sjögren’s syndrome. Clin Exp Immunol 169(1):17–26PubMedCentralPubMedCrossRefGoogle Scholar
  6. 6.
    Katsifis GE, Rekka S, Moutsopoulos NM et al (2009) Systemic and local interleukin-17 and linked cytokines associated with Sjögren’s syndrome immunopathogenesis. Am J Pathol 175(3):1167–1177PubMedCentralPubMedCrossRefGoogle Scholar
  7. 7.
    Nguyen CQ, Hu MH, Li Y et al (2008) Salivary gland tissue expression of interleukin-23 and interleukin-17 in Sjögren’s syndrome: findings in humans and mice. Arthritis Rheum 58(3):734–743PubMedCentralPubMedCrossRefGoogle Scholar
  8. 8.
    MacLennan IC (1994) Germinal centers. Annu Rev Immunol 12:117–139PubMedCrossRefGoogle Scholar
  9. 9.
    Risselada AP, Looije MF, Kruize AA et al (2013) The role of ectopic germinal centers in the immunopathology of primary Sjögren’s syndrome: a systematic review. Semin Arthritis Rheum 42(4):368–376PubMedCrossRefGoogle Scholar
  10. 10.
    Ohara T, Itoh Y, Itoh K (2000) Revaluation of laboratory parameters in relation to histological findings in primary and secondary Sjögren’s syndrome. Intern Med 39(6):457–463PubMedCrossRefGoogle Scholar
  11. 11.
    Le Pottier L, Devauchelle V, Fautrel A et al (2009) Ectopic germinal centers are rare in Sjogren’s syndrome salivary glands and do not exclude autoreactive B cells. J Immunol 182(6):3540–3547PubMedCrossRefGoogle Scholar
  12. 12.
    Wong CK, Lit LC, Tam LS et al (2008) Hyperproduction of IL-23 and IL-17 in patients with systemic lupus erythematosus: implications for Th17-mediated inflammation in autoimmunity. Clin Immunol 127:385–393PubMedCrossRefGoogle Scholar
  13. 13.
    Kim J, Kang S, Kim J et al (2013) Elevated levels of T helper 17 cells are associated with disease activity in patients with rheumatoid arthritis. Ann Lab Med 33(1):52–59PubMedCentralPubMedCrossRefGoogle Scholar
  14. 14.
    Nguyen CQ, Hu MH, Li Y et al (2008) Salivary gland tissue expression of interleukin-23 and interleukin-17 in Sjögren’s syndrome: findings in humans and mice. Arthritis Rheum 58:734–743PubMedCentralPubMedCrossRefGoogle Scholar

Copyright information

© Clinical Rheumatology 2014

Authors and Affiliations

  • Yunyun Fei
    • 1
  • Wen Zhang
    • 1
  • Dongfang Lin
    • 2
  • Chen Wu
    • 3
  • Mengtao Li
    • 1
  • Yan Zhao
    • 1
  • Xiaofeng Zeng
    • 1
  • Fengchun Zhang
    • 1
  1. 1.Department of RheumatologyPeking Union Medical College HospitalBeijingChina
  2. 2.Department of RheumatologyThe Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouChina
  3. 3.Department of RheumatologyHua Xin Hospital First Hospital of Tsinghua UniversityBeijingChina

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