In the absence of langerin<sup>+</sup> CD8α<sup>+</sup> DCs, the immune response to blood-borne BCG infection was diminished: bacterial numbers in the spleen increased, serum IL-12p40 decreased, and delayed CD8<sup>+</sup> T cell activation, proliferation, and IFN-γ production was evident.
Finally, Sppl2a<sup>-/-</sup> mice lack cDC2s, have CD4<sup>+</sup> T cells that produce small amounts of IFN-γ after BCG infection, and are highly susceptible to infection with BCG or Mycobacterium tuberculosis.
In conclusion, high dose IFNγ therapy in combination with antitubercular drugs led to resolution of BCG infection in a patient with dominant partial IFNγ deficiency.