非受体酪氨酸激酶信号在自身免疫中的作用及其治疗意义。
Non-receptor tyrosine kinase signaling in autoimmunity and therapeutic implications.
机构信息
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
出版信息
Pharmacol Ther. 2019 Sep;201:39-50. doi: 10.1016/j.pharmthera.2019.05.008. Epub 2019 May 11.
Autoimmune diseases are characterized by impaired immune tolerance towards self-antigens, leading to enhanced immunity to self by dysfunctional B cells and/or T cells. The activation of these cells is controlled by non-receptor tyrosine kinases (NRTKs), which are critical mediators of antigen receptor and cytokine receptor signaling pathways. NRTKs transduce, amplify and sustain activating signals that contribute to autoimmunity, and are counter-regulated by protein tyrosine phosphatases (PTPs). The function of and interaction between NRTKs and PTPs during the development of autoimmunity could be key points of therapeutic interference against autoimmune diseases. In this review, we summarize the current state of knowledge of the functions of NRTKs and PTPs involved in B cell receptor (BCR), T cell receptor (TCR), and cytokine receptor signaling pathways that contribute to autoimmunity, and discuss their targeting for therapeutic approaches against autoimmune diseases.
自身免疫性疾病的特征是对自身抗原的免疫耐受受损，导致功能失调的 B 细胞和/或 T 细胞对自身产生增强的免疫。这些细胞的激活受非受体酪氨酸激酶（NRTKs）的控制，NRTKs 是抗原受体和细胞因子受体信号通路的关键介质。NRTKs 转导、放大和维持激活信号，有助于自身免疫，并受蛋白酪氨酸磷酸酶（PTPs）的反向调节。在自身免疫的发展过程中，NRTKs 和 PTPs 的功能和相互作用可能是针对自身免疫性疾病进行治疗干预的关键点。在这篇综述中，我们总结了参与 B 细胞受体（BCR）、T 细胞受体（TCR）和细胞因子受体信号通路的 NRTKs 和 PTPs 的功能的最新知识，这些通路有助于自身免疫，并讨论了针对自身免疫性疾病的治疗方法的靶向性。
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