Figure 4. Ligand activation of RXR inhibits type I IFN and ISGs.

(a,b) RAW264.7 cells were pretreated with DMSO or 9cRA (100 nM) for 16 h and subsequently transfected with 1 μg ml⁻¹ polyI:C for 2 h. RNA was extracted and gene expression profile was detected by Affimetrix430.2 Chip. (a) PolyI:C-responsive genes which included polyI:C-inducible genes (DMSO-polyI:C/DMSO>2.0) and polyI:C-suppressed genes (DMSO-polyI:C/DMSO<0.5) were further analysed, the polyI:C-responsive genes can be divided into two groups, 9cRA-inducible polyI:C-responsive genes ((9cRA-polyI:C/DMSO)/(DMSO-polyI:C/DMSO)>2.0) and 9cRA-suppressed polyI:C-responsive genes ((9cRA-polyI:C/DMSO)/(DMSO-polyI:C/DMSO)<0.5). (b) Multiple type I IFN genes were 9cRA-suppressed polyI:C-responsive genes. (c) RAW264.7 cells were pretreated with DMSO, 9cRA (100 nM), or HX531(1 μM) for 16 h and subsequently transfected with 1 μgml⁻¹ polyI:C. RNA was collected 2 h after transfection, the mRNA expression of RXR target genes Abca1, Abcg1 and primary antiviral genes Ifnβ, Isg15 were measured by qPCR. (d) RAW264.7 cells were pretreated as described in c, mRNA expression of ISGs with known antiviral activity, Irf7, Oas2, Gbp1 and Isg20 were quantified by qPCR. Data of c,d are shown as mean ± s.d. (n = 3) of one representative experiment, similar results were obtained in three independent experiments. *P<0.05 and **P<0.01 (Student's t-test).