As expected, acute deletion of Uba3 did not affect the initial number and activation status (CD44hi) of splenic CD4+ T cells prior to parasite infection (Fig 5B), but led to impaired production of serum IFN-γ (Fig 5C), parasite-specific IgG responses (Fig 5D), splenic GC B cell formation (Fig 5E), and plasma cell differentiation (Fig 5F), which closely mimicked the defective anti-P. Here, IFNG is linked to parasitic infectious disease.