CXCL10 and infection: However, in contrast to these findings, our results show that knockdown of DHX35 significantly reduced the production of IFN-β, IL6 and CXCL10, and inhibited the activation of downstream signaling pathways after infection with RNA virus and transfection with cytosolic poly(I:C) and poly(dA:dT), whereas overexpression of DHX35 increased the production of IFN-β, IL6 and CXCL10 in human airway epithelial cells.