Although iBALT formation is reduced in the absence of Th2 or Th17, this model of immune response is not directly dependent on Th1, Th2, or Th17 responses [35], consistent with the lack of PCP susceptibility of mice specifically depleted in IFNγ, IL-4, and IL-17 cytokines [16,42,105]. The gene discussed is IL4; the disease is pneumocystosis.