Functional abnormalities in protein tyrosine phosphatase ε-deficient macrophages

Veronica Sully, Scott Pownall, Elizabeth Vincan, Sahar Bassal, Anita H. Borowski, Prue H. Hart, Steven P. Rockman, Wayne A. Phillips

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)184-188
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - 1 Jan 2001
Externally publishedYes


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