Our results showed that the SND1 mice contributed significantly to the development of Th1/17 protective immunity against the infection because the SND1-/- mice showed significantly higher body weight loss, greater organism growth, and much more severe pathological changes in the lung compared with wild-type mice, which were associated with reduced IFN-γ production by CD4+ and CD8+ T cells and increased Treg cells in SND1-/- mice. This evidence concerns the gene SND1 and infection.