In this study, we found that mice lacking IFNAR could be partially resistant to T. gondii PRU intraperitoneal infection, which was different from the chronic oral infection, and mice administered with recombinant IFN-I displayed to be more susceptible to this parasite infection, indicating IFN-I is detrimental to the hosts ability to generate anti-T. gondii immune responses. This evidence concerns the gene IFNAR1 and infection.