PLSCR2 deficiency in the IFN-I-induced antiviral and inflammatory gene signature

Phospholipid scramblase 2 (PLSCR2) plays an negative role in type I IFN responses. PLSCR2 constitutively interacts with STAT3, and PLSCR2 deficiency enhances IFN-I-induced gene expression and antiviral activity in an STAT3-dependent manner. We used microarrays to compare the overall difference of intrinsic and IFN-induced gene expression between wild-type and PLSCR2 deficient cells PLSCR2 knockout (PLS2KO) cells were generated from immortalized hepatocyte cell line ML-1. In this study, wild-type and PLS2KO ML-1 cells were treated with mouse IFN-α4 in 1000U/ml for 6 hours to compare their antiviral and inflammatory gene signature by using the affymetrix Mouse Clariom S Array platform.