Immune subversion by Helicobacter pylori.
To maintain prolonged colonization of the human gastric mucosa, Helicobacter pylori must avoid both innate and adaptive immune responses. During its long coexistence with humans, it has evolved complex strategies to maintain a mild inflammation of the gastric epithelium while limiting the extent of immune effector activity. Severe disease, associated with bacterial colonization, might reflect loss of this control. Several mechanisms and the bacterial factors involved in immune subversion have, in recent years, been elucidated, thus opening the possibility of a better understanding of the pathogenicity of this microorganism.
Baldari
Cosima T
CT
Department of Evolutionary Biology, University of Siena, Via A. Moro 2, I-53100 Siena, Italy. baldari@unisi.it
Lanzavecchia
Antonio
A
Telford
John L
JL
D017951:Antigen Presentation; D001402:B-Lymphocytes / Q000276:immunology; D001428:Bacterial Vaccines / Q000302:isolation & purification; D005753:Gastric Mucosa / Q000276:immunology / Q000382:microbiology; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology; D016480:Helicobacter pylori / Q000276:immunology* / Q000472:pathogenicity*; D006801:Humans; D007113:Immunity, Innate; D018448:Models, Immunological; D009569:Nitric Oxide / Q000378:metabolism; D010587:Phagocytosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology; D014774:Virulence
D001428:Bacterial Vaccines; D017382:Reactive Oxygen Species; D009569:Nitric Oxide