Cytotoxic T cells in H. pylori-related gastric autoimmunity and gastric lymphoma.

Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop gastric B-cell lymphoma, gastric autoimmunity, or other life threatening diseases, as gastric cancer or peptic ulcer. The type of host immune response against H. pylori, p...

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Publicado en:Journal of Biomedicine & Biotechnology pp. 10p - 11
Autores principales: Bergman MP, D'Elios MM
Formato: pictorial review tables/charts Journal Article
Publicado: Wiley-Blackwell 2010
Acceso en línea:Ver este registro en EBSCOhost
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        atl: Cytotoxic T cells in H. pylori-related gastric autoimmunity and gastric lymphoma.
      aug:
        au:
          Bergman MP
          D'Elios MM
        affil: Section Molecular Microbiology, Department of Molecular Cell Biology, VU University, 1081 HV, Amsterdam, The Netherlands.
      sug:
        subj:
          Gastrointestinal System
          Helicobacter Pylori
          Immunity
          Lymphoma
          T Lymphocytes
          Antigens
          Helicobacter Infections
          Proteins
          Ulcer
      ab: Helicobacter pylori infection is the major cause of gastroduodenal pathologies, but only a minority of infected patients develop gastric B-cell lymphoma, gastric autoimmunity, or other life threatening diseases, as gastric cancer or peptic ulcer. The type of host immune response against H. pylori, particularly the cytolytic effector functions of T cells, is crucial for the outcome of the infection. T cells are potentially able to kill a target via different mechanisms, such as perforins or Fas-Fas ligand interaction. In H. pylori-infected patients with gastric autoimmunity cytolytic T cells, that cross-recognize different epitopes of H. pylori proteins and H(+)K(+)-ATPase autoantigen, infiltrate the gastric mucosa and lead to gastric atrophy via long-lasting activation of Fas ligand-mediated appotosis and perforin-induced cytotoxicity. On the other hand, gastric T cells from MALT lymphoma exhibit defective perforin- and Fas-Fas ligand-mediated killing of B cells, with consequent abnormal help for B-cell proliferation, suggesting that deregulated and exhaustive H. pylori-induced T cell-dependent B-cell activation can support both the onset and the promotion of low-grade B-cell lymphoma.
      pubtype: Academic Journal
      doctype:
        pictorial
        review
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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