In this model, ɣδ and CD8+ T cells did not influence the course of infection.79 In another study, ILC1s were potent IFN-ɣ and TNF producers and participated in the control of T. gondii infection.90 Mice lacking the ILC1-master transcription factor T-bet or alymphoid Rag2−/−Il2rɣ−/− mice had higher T. gondii loads than WT animals and recruited less inflammatory monocytes into the small intestine.90 Adoptive transfer of ILC1s into Rag2−/−Il2rɣ−/− mice decreased parasite burden and significantly enhanced monocyte infiltration. This evidence concerns the gene IFNA1 and infection.