Abstract: Objective To investigate the role of interferon inducible protein IFI 16 and JAK-STAT pathway in the pathogenesis of systemic lupus erythematosus(SLE).Methods The peripheral blood mononuclear cells (PBMCs) isolated from 35 SLE patients and 16 normal controls were subjected either to detection of the mRNA expression of IFI16,or to culture in vitro,pretreated with AG490 to block the JAK-STAT pathway,and then deteced by RT-PCR for the expression of IFI 16 mRNA.Results The mean expression level of IFI 16 mRNA was significantly higher in both active SLE group and inactive SLE group than that in normal controls (P<0.001).No statistical difference was found in IFI 16 mRNA expression between the active and inactive SLE group (P>0.05).After the JAK-STAT pathway was blocked by AG490,the expression of IFI 16 mRNA were significantly decreased in active and inactive SLE group (P<0.001),but remained unchanged in normal controls (P>0.05).Conclusion The overexpression of IFI 16 gene in patients with SLE indicates that it might be a causative gene of SLE.

Key words: Lupus erythematosus, systemic, IFI 16, JAK-STAT pathway