Accordingly, mice that lack IFNγ do not develop gland hyperplasia or metaplasia in response to infection; this pro-inflammatory cytokine produced by CD4+ CD25− Th cells is crucial for the control of Helicobacter infection on the one hand and induces preneoplastic changes in the gastric mucosa on the other hand [36]. Here, IFNG is linked to Helicobacter pylori infectious disease.