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Atorvastatin restores imbalance of cluster of differentiation 4 (CD4)+ T cells in immune thrombocytopenia in vivo and in vitro

PI3K/AKT/mTOR通路 蛋白激酶B 激酶 MAPK/ERK通路 免疫系统 癌症研究 细胞生物学 蛋白激酶A 免疫学 生物 信号转导
作者
Pengcheng Xu,Yajing Zhao,Tengbo Yu,Yonghua Yu,Xiaofei Ni,Haoyi Wang,Lu Sun,Panpan Han,Lingjun Wang,Tao Sun,Xinguang Liu,Hai Zhou,Jun Peng,Ming Hou,Yu Hou,Miao Xu
出处
期刊:British Journal of Haematology [Wiley]
卷期号:201 (3): 530-541 被引量:7
标识
DOI:10.1111/bjh.17938
摘要

Immune thrombocytopenia (ITP) is an autoimmune haemorrhagic disease, in which the overactivation of T cells is crucial in the pathogenesis. Atorvastatin (AT), a lipid-lowering medicine, has shown promising immunomodulatory effects in certain inflammatory conditions. However, the immunoregulatory role of AT in ITP remains elusive. To investigate the effect of AT in the treatment of ITP, cluster of differentiation 4 (CD4)+ T cells were isolated from patients with ITP and cultured with different dosages of AT. We found that AT significantly inhibited cell proliferation, led to cell cycle arrest, induced apoptosis, and repressed the activation of CD4+ T cells in vitro. ITP murine models were then established, and results showed that AT treatment led to faster recovery of the platelet count to normal and exhibited comparable immunomodulatory function. Furthermore, we found the phosphorylation of mammalian target of rapamycin (mTOR), protein kinase B (AKT) and extracellular signal-regulated kinase (ERK), as well as activation of rat sarcoma virus (RAS) were all reduced dramatically after AT treatment in vitro. In conclusion, our present study demonstrated that AT could reinstate the functions of CD4+ T cells by inhibiting the excessive activation, proliferation, and survival of CD4+ T cells in ITP via the RAS/mitogen-activated protein kinase kinase (MEK)/ERK and the mTOR/phosphatidylinositol-3 kinase (PI3K)/AKT pathway. Therefore, we propose that AT could be used as a potential therapeutic option for ITP by restoring the over-activated cellular immunity.
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