Immune response to Helicobacter pylori infection and gastric cancer development

Table 1 Roles of Helicobacter pylori virulence factors on host immune response

Virulence factor	Effects over immune response	Ref.
CagA	IL-8 stimulation; Suppression of proinflammatory cytokines through the inhibition of MAPK and NF-κB	Schumacher and Schwarz[81] and Garlanda et al[83]
VacA	Inhibition of activation and proliferation of T and B cells; Induction of the apoptosis of macrophages (inhibition of INF-β signaling); IL-8 stimulation; Inhibition of IL-2 production by inhibiting NFAT; Impairment of antigen presentation by B lymphocytes	Drici et al[86] Dinarello[89], Hollegaard and Bidwell[90], Sicinschi et al[91] and Garza-González et al[92]
DupA	Promotion of neutrophilic infiltration	Zeng et al[94]
OipA	Promotion of neutrophilic infiltration; Stimulation of IL-1, IL-6, IL-8, IL-11, IL-17, MMP-1, TNF-α, and IRF-1	Gehmert et al[97]
IceA	Stimulation of IL-1, IL-6, and IL-8	Abbasian et al[101]
BabA	Stimulation of IL-33	Xue et al[108]

BabA: Blood group antigen-binding adhesin; DupA: Duodenal ulcer promoter A; IL: Interleukin; INF-β: Interferon-beta; IRF-1: Interferon regulatory factor 1; MAPK: Mitogen-activated protein kinase; MMP-1: Matrix metalloproteinase-1; NF-κB: Nuclear factor-κB; NFAT: Nuclear factor of activated T-cells; OipA: External inflammatory protein A; TNF: Tumor necrosis factor; VacA: Vacuolating cytotoxin A.