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Li, H., Fu, Y.X., Wu, Q., Zhou, Y., Crossman, D.K., Yang, P., Li, J., Luo, B., Morel, L.M., Kabarowski, J.H., Yagita, H., Ware, C.F., Hsu, H.C. and Mountz, J.D. (2015) Interferon-Induced Mechanosensing Defects Impede Apoptotic Cell Clearance in Lupus. The Journal of Clinical Investigation, 125, 2877-2890.
https://doi.org/10.1172/JCI81059

has been cited by the following article:

• TITLE: LXR, PPARγ, and PPARδ Agonists Are Not Sufficient to Demonstrate Therapeutic Potential against Mouse Model of Systemic Lupus Erythematosus

  AUTHORS: Noriko Toyota Tatebe, Katsue Sunahori Watanabe, Sonia Zeggar, Sumie Hiramatsu, Minglu Yan, Takayuki Katsuyama, Eri Katsuyama, Haruki Watanabe, Ken-ei Sada, Jun Wada

  KEYWORDS: Nuclear Receptors, Liver X Receptor (LXR), Peroxisome Proliferator-Activated Receptor (PPAR), Systemic Lupus Erythematosus (SLE)

  JOURNAL NAME: Open Journal of Rheumatology and Autoimmune Diseases, Vol.7 No.2, May 31, 2017

  ABSTRACT: Aim: We aimed to investigate whether the agonists for liver X receptor (LXR) ameliorate lupus-like phenotypes in mice mediated by the clearance of apoptotic cells, and compare with peroxisome proliferator-activated receptor (PPAR) γ plus PPARδ agonists, which also facilitate the clearance of apoptotic cells and exert anti-inflammatory effects in systemic lupus erythematosus (SLE). Methods: We investigated the efficacy of LXR agonist (GW3965) or dual treatment of PPARγ (pioglitazone) and PPARδ (GW0742) agonists in SLE animal models, female MRL/MpJ-Fas/J mice and BALB/cAJcl mice treated with pristane. The data were analyzed with one-way analysis of variance and Tukey’s honestly significant difference tests. Results: The treatment with LXR or PPARγ/δ agonists did not significantly alter the swelling of lymph nodes, ds-DNA production, albuminuria, histological score of glomerular lesions, and mRNA expression of target genes including Abca1, C1qa, Icam1, Mertk and Tnf. Conclusion: LXR or PPARγ/δ agonists targeting the impaired clearance for apoptosis cells may not be efficient in the remission induction therapy in SLE.