More precisely, we observe loss of macrophages, but not CD4+ T-cells, significantly increases the production of IFN-γ by CD8+ T-cells and drives CD8+ T-cells toward a terminally differentiated effector memory phenotype [a cellular phenotype characterized by high levels of IFN-γ production (17)], all of which suggest that CD8+ T-cells upregulate IFN-γ responses to combat Pneumocystis infection during a secondary immune response. This evidence concerns the gene CD8A and Pneumocystis infectious disease.