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Hydroxychloroquine inhibits CD154 expression in CD4+ T lymphocytes of systemic lupus erythematosus through NFAT, but not STAT5, signaling

  • Wu, Shu-Fen1
  • Chang, Chia-Bin1
  • Hsu, Jui-Mei2, 3
  • Lu, Ming-Chi2, 4, 3
  • Lai, Ning-Sheng2, 4, 3
  • Li, Chin1
  • Tung, Chien-Hsueh1, 2
  • 1 National Chung-Cheng University, Department of Life Science, Institute of Molecular Biology, No.168, University Rd, Min-Hsiung, Chia-Yi, 62247, Taiwan , Min-Hsiung, Chia-Yi (Taiwan)
  • 2 Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Division of Allergy, Immunology and Rheumatology, Chia-Yi, Taiwan , Chia-Yi (Taiwan)
  • 3 Department of Medical Research, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Dalin, Chia-Yi, Taiwan , Dalin, Chia-Yi (Taiwan)
  • 4 Tzu Chi University, College of Medicine, Hualien, Taiwan , Hualien (Taiwan)
Published Article
Arthritis Research & Therapy
Springer Science and Business Media LLC
Publication Date
Aug 09, 2017
DOI: 10.1186/s13075-017-1393-y
Springer Nature


BackgroundOverexpression of membranous CD154 in T lymphocytes has been found previously in systemic lupus erythematosus (SLE). Because hydroxychloroquine (HCQ) has been used frequently in the treatment of lupus, we sought to identify the effects of HCQ on CD154 and a possibly regulatory mechanism.MethodsCD4+ T cells were isolated from the blood of lupus patients. After stimulation with ionomycin or IL-15 and various concentrations of HCQ, expression of membranous CD154 and NFAT and STAT5 signaling were assessed.ResultsHCQ treatment had significant dose-dependent suppressive effects on membranous CD154 expression in ionomycin-activated T cells from lupus patients. Furthermore, HCQ inhibited intracellular sustained calcium storage release, and attenuated the nuclear translocation of NFATc2 and the expression of NFATc1. However, CD154 expressed through IL-15-mediated STAT5 signaling was not inhibited by HCQ treatment.ConclusionsHCQ inhibited NFAT signaling in activated T cells and blocked the expression of membranous CD154, but not STAT5 signaling. These findings provide a mechanistic insight into SLE in HCQ treatment.

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