Protein tyrosine phosphatase ε (PTPε)-deficient mice were generated by targeted deletion of exons 3, 4, and 5 of the Ptpre gene. Mice homozygous for this deletion (PtpreΔ3.5) were fertile, bred and developed normally and exhibited no overt phenotype. However, closer examination of the function of macrophages from these mice revealed a defect in the regulation of the respiratory burst. While bacterial lipopolysaccharide (LPS) or tumour necrosis factor α (TNFα) were able to prime bone marrow-derived macrophages (BMM) from wild type (Ptpre+) macrophages for an enhanced respiratory burst, they were unable to do so in macrophages from PTPε-deficient mice. PTPε-deficient BMM also had abnormalities in cytokine production with a reduced ability to produce TNFα and enhanced IL-10 production in response to challenge with LPS. These findings suggest an important role for PTPε in the control of macrophage function.
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - 1 Jan 2001|