B6 sjl cd45.1 mice

C57BL/6 mice were purchased from Orient. Rorgt^gfp/gfp , OT-II and B6.SJL (CD45.1⁺) mice were purchased from Jackson Laboratory. OT-II mice were crossed with B6.SJL for adoptive transfer study. All mice were maintained under the semi-specific-pathogen-free facility in an animal center (Seoul National University). All animal experiments were performed using a protocol approved by the Institutional Animal Care and Use Committee Seoul National University (SNU-140602-2-10).

C57BL/6N (WT) mice were either purchased from Charles River or bred in-house. No differences in survival or disease progression during Mtb infection were observed in Irg1^+/+ littermate controls or Irg1^+/+ C57BL/6N mice obtained from Charles River in three independent experiments. B6.SJL (CD45.1) mice were obtained from Jackson Laboratories. Irg1^−/− mice (embryonic stem cells obtained from KOMP [C57BL/6N background, reporter-tagged insertion with conditional potential, MGI: 103206]) were generated at Washington University and have been described previously (Lampropoulou et al., 2016 (link)). Adult mice (6–13 wk of age) of both sexes were used, and sex was randomized between experiments. Cre⁻Irg1^fl/fl mice were generated as described previously (Coleman et al., 2015 (link)) with two loxP sites flanking exon 4 of Irg1. Irg1^−/− mice were bred with FLPe “deleter” mice (Kanki et al., 2006 (link)) to facilitate deletion of lacZ and neomycin resistance cassettes between FRT sites and create Irg1^fl/+ founder mice. The founder mice were backcrossed to C57BL6/J background using speed congenic approaches (>99% purity) and then interbred to generate Irg1^fl/fl mice. These animals were crossed with Mrp8-Cre⁺–, LysM-Cre⁺– and CD11c-Cre⁺–(Jackson Laboratory) expressing mice to delete exon 4 of Irg1 from specific subsets of myeloid cells.