Some studies have shown that the response of T helper cells to infection with H. pylori is polarized, as the T CD4+ cells in the gastric mucosa of infected individuals produce proinflammatory cytokines Th1 such as IL-12, and INF-γ, whereas Th2 regulatory cytokines such as IL-4 are absent in H. pylori infection (116, 117). Here, CD4 is linked to infection.