Shp1 function in myeloid cells. Issue 3 (12th June 2017)

• Record Type: Journal Article
• Authors: Abram, Clare L.; Lowell, Clifford A.
• Is Part Of: Journal of leukocyte biology. Volume 102:Issue 3(2017)
• Page Start: 657
• Page End: 675
• Publication Date: 2017-06-12
• Subjects: motheaten -- inflammation -- autoimmunity -- tyrosine phosphatase -- Ptpn6; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1189/jlb.2MR0317-105R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract : Review on the role of Shp1, and how myeloid‐specific dysregulation may contribute to disease. Abstract : The motheaten 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.