Deletion of the Alzheimer's Disease-associated CD33 results in increased phagocytosis, oxidative burst and inflammation

In this study, wild type and CD33 knockout human THP1 macrophages were treated with control shRNA or shRNA against the CD33 signaling-associated protein tyrosine phosphatase PTPN6 and analyzed by mRNA sequencing. Whole genome transcriptome analysis showed that knockout of CD33 as well as knockdown of PTPN6 led to constitutive activation of inflammation-related pathways. On the other hand, PTPN6 knockdown was associated with changes in cell cycle and mitosis-related pathways in a CD33-deficient background. Overall design: Examination of mRNA profiles of THP1 macrophages after knockout of CD33 and/or knockdown of PTPN6 by RNA-Seq (6 samples per group).