Role of the transcription factor Fli-1 on the CXCL10/CXCR3 Axis*

The transcription factor Fli-1, a member of the ETS family factors, is implicated in pathogenesis lupus disease. Reduced Fli-1 expression mice leads to decreased renal Cxcl10 mRNA levels and infiltrating CXCR3+ T cells that parallels reduced inflammatory cell infiltration damage. Inflammatory chemokine CXCL10 critical for attracting expressing receptor CXCR3. CXCL10/CXCR3 axis plays role various diseases including lupus. Our data here demonstrate protein are significantly lower heterozygous MRL/ lpr compared wild-type mice. Knockdown secretion mouse human endothelial cells, mesangial upon LPS or TNFα stimulation. inhibitor, Camptothecin, production monocyte interferon Four putative Ets binding sites promoter showed significant enrichment FLI-1; however, FLI-1 did not directly drive from promoters, suggesting may regulate indirectly. results also suggest DNA domain necessary regulation hCXCR3 promotor activity interactions with co-activators. Together, these support modulating CXCL10-CXCR3 by indirectly regulating both genes impact disease development. Signaling pathways drugs reduce offer novel approaches treatment.