Fig. 2

Molecular and cellular features associated with helicobacter pylori-induced gastric carcinogenesis. A Direct impacts that cause uncontrolled cell proliferation and DNA damage are caused by bacterial effectors such cagA, vacA, and omp. CagA phosphorylation arises by host’s Src/Abl kinases and the phosphorylated CagA stimulates a series of signaling molecules like PI3K/Akt, Ras, Raf, ERK, JAK/STAT, and βcatenin. B When the H. pylori reaches to submucosa, DCs capture and present the antigens to the naive T cell and define the outcome of immune responses. According to the cytokine pattern in the bacterial microenvironment, T cells differentiate into TH1 and TH17 phenotypes which induces the inflammatory response. TH17 more also induces MMPs through IL-17. In contrast, secreted IL-2 from DCs promote Tregs differentiation and in turns suppresses the effective immune responses by secreting IL-10 and so, preserving H. pylori inside the gastric mucosa. IL: Interleukin; TNF: Tumor necrosis factor; Cag A: Cytotoxin associated gene A; Vac A:Vacuolating cytotoxin A; JAK: Janus kinase; STAT:Signal transducer and activator of transcription; Ras:Rat sarcoma; Raf:Rapidly accelerated fibrosarcoma; ERK: Extracellular signal-regulated kinase; PI3K: Phosphatidylinositol 3-kinase; Akt: Protein kinase B; MMPs: Matrix metalloproteinases; Omp: outer membrane protein