布鲁顿酪氨酸激酶在自身免疫中的作用及治疗意义。
The role of Bruton's tyrosine kinase in autoimmunity and implications for therapy.
作者信息
Crofford Leslie J, Nyhoff Lindsay E, Sheehan Jonathan H, Kendall Peggy L
机构信息
a Division of Rheumatology & Immunology, Department of Medicine , Vanderbilt University , Nashville , TN , USA.
b Department of Pathology, Microbiology & Immunology , Vanderbilt University , Nashville , TN , USA.
出版信息
Expert Rev Clin Immunol. 2016 Jul;12(7):763-73. doi: 10.1586/1744666X.2016.1152888. Epub 2016 Mar 4.
Bruton's tyrosine kinase (BTK) mediates B cell signaling and is also present in innate immune cells but not T cells. BTK propagates B cell receptor (BCR) responses to antigen-engagement as well as to stimulation via CD40, toll-like receptors (TLRs), Fc receptors (FCRs) and chemokine receptors. Importantly, BTK can modulate signaling, acting as a "rheostat" rather than an "on-off" switch; thus, overexpression leads to autoimmunity while decreased levels improve autoimmune disease outcomes. Autoreactive B cells depend upon BTK for survival to a greater degree than normal B cells, reflected as loss of autoantibodies with maintenance of total antibody levels when BTK is absent. This review describes contributions of BTK to immune tolerance, including studies testing BTK-inhibitors for treatment of autoimmune diseases.
布鲁顿酪氨酸激酶（BTK）介导B细胞信号传导，也存在于固有免疫细胞中，但不存在于T细胞中。BTK将B细胞受体（BCR）对抗原结合以及通过CD40、Toll样受体（TLR）、Fc受体（FCR）和趋化因子受体的刺激反应进行信号传导。重要的是，BTK可以调节信号传导，起到“变阻器”而非“开关”的作用；因此，过度表达会导致自身免疫，而水平降低则会改善自身免疫性疾病的结果。自身反应性B细胞比正常B细胞在更大程度上依赖BTK来存活，这表现为当缺乏BTK时自身抗体丧失而总抗体水平维持。本综述描述了BTK对免疫耐受的作用，包括测试BTK抑制剂治疗自身免疫性疾病的研究。
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