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本文引用的文献

1
Increased expression of Mer tyrosine kinase in circulating dendritic cells and monocytes of lupus patients: correlations with plasma interferon activity and steroid therapy.狼疮患者循环树突状细胞和单核细胞中Mer酪氨酸激酶表达增加:与血浆干扰素活性及类固醇治疗的相关性
Arthritis Res Ther. 2014 Mar 21;16(2):R76. doi: 10.1186/ar4517.
2
Circulating levels of soluble MER in lupus reflect M2c activation of monocytes/macrophages, autoantibody specificities and disease activity.狼疮中可溶性MER的循环水平反映了单核细胞/巨噬细胞的M2c活化、自身抗体特异性和疾病活动度。
Arthritis Res Ther. 2013;15(6):R212. doi: 10.1186/ar4407.
3
Lck availability during thymic selection determines the recognition specificity of the T cell repertoire.在胸腺选择过程中 Lck 的可用性决定了 T 细胞 repertoire 的识别特异性。
Cell. 2013 Sep 12;154(6):1326-41. doi: 10.1016/j.cell.2013.08.009.
4
Spleen tyrosine kinase (Syk) regulates systemic lupus erythematosus (SLE) T cell signaling.脾酪氨酸激酶(Syk)调节系统性红斑狼疮(SLE)T 细胞信号转导。
PLoS One. 2013 Aug 27;8(8):e74550. doi: 10.1371/journal.pone.0074550. eCollection 2013.
5
Bruton's tyrosine kinase mediates the synergistic signalling between TLR9 and the B cell receptor by regulating calcium and calmodulin.布鲁顿酪氨酸激酶通过调节钙和钙调蛋白介导 TLR9 和 B 细胞受体之间的协同信号转导。
PLoS One. 2013 Aug 14;8(8):e74103. doi: 10.1371/journal.pone.0074103. eCollection 2013.
6
Ibrutinib and novel BTK inhibitors in clinical development.伊布替尼和处于临床开发阶段的新型 BTK 抑制剂。
J Hematol Oncol. 2013 Aug 19;6:59. doi: 10.1186/1756-8722-6-59.
7
Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation.树突状细胞中 MyD88 的过度激活信号,通过 Lyn 激酶的特异性缺失,导致严重的自身免疫和炎症。
Proc Natl Acad Sci U S A. 2013 Aug 27;110(35):E3311-20. doi: 10.1073/pnas.1300617110. Epub 2013 Aug 12.
8
T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response.T 细胞衍生蛋白 S 通过与树突状细胞中的 TAM 受体信号相互作用来控制免疫反应的幅度。
Immunity. 2013 Jul 25;39(1):160-70. doi: 10.1016/j.immuni.2013.06.010. Epub 2013 Jul 11.
9
Suppression of glomerulonephritis in lupus-prone NZB × NZW mice by RN486, a selective inhibitor of Bruton's tyrosine kinase.布鲁顿酪氨酸激酶选择性抑制剂RN486对狼疮易感NZB×NZW小鼠肾小球肾炎的抑制作用
Arthritis Rheum. 2013 Sep;65(9):2380-91. doi: 10.1002/art.38047.
10
Inhibitors of BTK and ITK: state of the new drugs for cancer, autoimmunity and inflammatory diseases.BTK 和 ITK 抑制剂:用于癌症、自身免疫和炎症性疾病的新药现状。
Scand J Immunol. 2013 Aug;78(2):130-9. doi: 10.1111/sji.12069.

酪氨酸激酶在系统性红斑狼疮中的作用及其作为治疗靶点的潜力。

The role of tyrosine kinases in systemic lupus erythematosus and their potential as therapeutic targets.

机构信息

Department of Medicine and Temple Autoimmunity Center, Section of Rheumatology, Temple University, Philadelphia, PA, USA.

出版信息

Expert Rev Clin Immunol. 2014 May;10(5):573-82. doi: 10.1586/1744666X.2014.893827. Epub 2014 Mar 29.

DOI:10.1586/1744666X.2014.893827
PMID:24678775
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4249585/
Abstract

The autoimmune disease systemic lupus erythematosus is characterized by loss of tolerance to nuclear antigens. Breakdown of tolerance is associated with alterations in T-cell and B-cell receptor signal transduction, including increased protein phosphorylation that may underlie pathogenesis and explain the characteristic hyperactivity of T and B cells and other immune cells in active disease. Tyrosine kinases play a central role in signaling processes in cells known to be important in the pathogenesis of autoimmune diseases. Considerable progress has been made in understanding the function of tyrosine kinases in immune cell signaling pathways. In this review, we will summarize the function of tyrosine kinases and their novel inhibitors from studies made in animal lupus models and systemic lupus erythematosus patients.

摘要

自身免疫性疾病系统性红斑狼疮的特征是对核抗原失去耐受性。耐受性的破坏与 T 细胞和 B 细胞受体信号转导的改变有关,包括蛋白磷酸化增加,这可能是发病机制的基础,并解释了活动期疾病中 T 和 B 细胞及其他免疫细胞的特征性过度活跃。酪氨酸激酶在已知对自身免疫性疾病发病机制重要的细胞信号转导过程中发挥核心作用。在理解酪氨酸激酶在免疫细胞信号通路中的功能方面已经取得了相当大的进展。在这篇综述中,我们将总结在动物狼疮模型和系统性红斑狼疮患者研究中发现的酪氨酸激酶及其新型抑制剂的功能。