Our data is consistent with some studies from other investigators: Carmona et al. found that β-glucan surface components of Pneumocystis drive the activation of the IL-23/IL-17 axis, thus stimulating Th17 cell immunity in infected mice [13]; using a nude mouse model, Hu et al. verified that deficiency in IFN-γ promoted the differentiation of Th17 cells and IL-17 is essential for inflammatory responses in PCP [35]; Ripamonti et al. noted that IL-17+γδ T cells and CD4+ T cells in the lungs were increased during Pneumocystis infection in immunocompetent mice. This evidence concerns the gene IFNG and Pneumocystis infectious disease.