In vivo studies on a NZB/W F1 murine model of lupus showed that HCQ in combination with PRD (2.5 mg/kg/day and 1 mg/kg/day p.o.) decreased autoantibody production, as well as being able to inhibit toll-like receptor activation, resulting in the down-regulation of type I interferon (IFN-α) which is deeply implicated in lupus pathogenesis.