Abram Clare L, Lowell Clifford A
Department of Laboratory Medicine and Immunology Program, University of California, San Francisco, California, USA.
Department of Laboratory Medicine and Immunology Program, University of California, San Francisco, California, USA
J Leukoc Biol. 2017 Sep;102(3):657-675. doi: 10.1189/jlb.2MR0317-105R. Epub 2017 Jun 12.
The mouse was first described in 1975 as a model of systemic inflammation and autoimmunity, as a result of immune system dysregulation. The phenotype was later ascribed to mutations in the cytoplasmic tyrosine phosphatase Shp1. This phosphatase is expressed widely throughout the hematopoietic system and has been shown to impact a multitude of cell signaling pathways. The determination of which cell types contribute to the different aspects of the phenotype caused by global Shp1 loss or mutation and which pathways within these cell types are regulated by Shp1 is important to further our understanding of immune system regulation. In this review, we focus on the role of Shp1 in myeloid cells and how its dysregulation affects immune function, which can impact human disease.
1975年，小鼠首次被描述为一种系统性炎症和自身免疫的模型，这是免疫系统失调的结果。该表型后来被归因于细胞质酪氨酸磷酸酶Shp1的突变。这种磷酸酶在整个造血系统中广泛表达，并已被证明会影响多种细胞信号通路。确定哪些细胞类型导致了由Shp1整体缺失或突变引起的表型的不同方面，以及这些细胞类型内的哪些通路受Shp1调节，对于加深我们对免疫系统调节的理解很重要。在这篇综述中，我们重点关注Shp1在髓系细胞中的作用，以及其失调如何影响免疫功能，而这可能会影响人类疾病。
