187 research outputs found
Recherches sur le plancton de la mer flamande (mer du Nord méridionale): I. Quelques flagellés, protistes et "caetera"
Recherches sur le plancton de la mer flamande (mer du Nord méridionale): II. <i>Biddulphiaeae</i>, <i>Proteomyxa</i>, <i>Rhizomastigina</i>, <i>Heliozoa</i>, <i>Amoebina</i>
Salomé.
Transcript of SALOMÉ by Maurice Kufferath, appearing in LE GUIDE MUSICAL, 24 mars 1907, pp. 227-9. (Strauss
Algues et protistes du fleuve Congo dans le Bas-Congo et de son estuaire - Première et deuxième partie
Algues et Protistes du fleuve Congo dans le Bas-Congo et de son estuaire: 2. Algues et protistes prélevés au large et dans la crique de Banana
Algues et Protistes du fleuve Congo dans le Bas-Congo et de son estuaire: 1. Algues et protistes du fleuve Congo au large de l'île de Mateba
Recherches sur les eaux saumâtres des environs de Lilloo: II. Partie descriptive. Algues et protiste. Considérations écologiques
Immune evasion by proteolytic shedding of natural killer group 2, member D ligands in Helicobacter pylori infection
[Background]: Helicobacter pylori (H. pylori) uses various strategies that attenuate mucosal immunity to ensure its persistence in the stomach. We recently found evidence that H. pylori might modulate the natural killer group 2, member 2 (NKG2D) system. The NKG2D receptor and its ligands are a major activation system of natural killer and cytotoxic T cells, which are important for mucosal immunity and tumor immunosurveillance. The NKG2D system allows recognition and elimination of infected and transformed cells, however viruses and cancers often subvert its activation. Here we aimed to identify a potential evasion of the NKG2D system in H. pylori infection.[Methods]: We analyzed expression of NKG2D system genes in gastric tissues of H. pylori gastritis and gastric cancer patients, and performed cell-culture based infection experiments using H. pylori isogenic mutants and epithelial and NK cell lines.[Results]: In biopsies of H. pylori gastritis patients, NKG2D receptor expression was reduced while NKG2D ligands accumulated in the lamina propria, suggesting NKG2D evasion. In vitro, H. pylori induced the transcription and proteolytic shedding of NKG2D ligands in stomach epithelial cells, and these effects were associated with specific H. pylori virulence factors. The H. pylori-driven release of soluble NKG2D ligands reduced the immunogenic visibility of infected cells and attenuated the cytotoxic activity of effector immune cells, specifically the anti-tumor activity of NK cells.[Conclusion]: H. pylori manipulates the NKG2D system. This so far unrecognized strategy of immune evasion by H. pylori could potentially facilitate chronic bacterial persistence and might also promote stomach cancer development by allowing transformed cells to escape immune recognition and grow unimpeded to overt malignancy.Supported by the Austrian Science Fund (FWF, DK-MOLIN W1241 and the “Cluster of Excellence: Microbiomes Drive Planetary Health”) and by the Spanish Ministry of Science and Innovation under Grants (PID2021-123795OB-I00, PID2020-115506RB-I00) [Ministerio de Ciencia, Innovación y Universidades (MCIU)/Agencia Estatal de Investigación (AEI)/European Regional Development Fund (FEDER, EU)].Peer reviewe
Immune evasion by proteolytic shedding of natural killer group 2, member D ligands in Helicobacter pylori infection
BackgroundHelicobacter pylori (H. pylori) uses various strategies that attenuate mucosal immunity to ensure its persistence in the stomach. We recently found evidence that H. pylori might modulate the natural killer group 2, member 2 (NKG2D) system. The NKG2D receptor and its ligands are a major activation system of natural killer and cytotoxic T cells, which are important for mucosal immunity and tumor immunosurveillance. The NKG2D system allows recognition and elimination of infected and transformed cells, however viruses and cancers often subvert its activation. Here we aimed to identify a potential evasion of the NKG2D system in H. pylori infection.MethodsWe analyzed expression of NKG2D system genes in gastric tissues of H. pylori gastritis and gastric cancer patients, and performed cell-culture based infection experiments using H. pylori isogenic mutants and epithelial and NK cell lines.ResultsIn biopsies of H. pylori gastritis patients, NKG2D receptor expression was reduced while NKG2D ligands accumulated in the lamina propria, suggesting NKG2D evasion. In vitro, H. pylori induced the transcription and proteolytic shedding of NKG2D ligands in stomach epithelial cells, and these effects were associated with specific H. pylori virulence factors. The H. pylori-driven release of soluble NKG2D ligands reduced the immunogenic visibility of infected cells and attenuated the cytotoxic activity of effector immune cells, specifically the anti-tumor activity of NK cells.ConclusionH. pylori manipulates the NKG2D system. This so far unrecognized strategy of immune evasion by H. pylori could potentially facilitate chronic bacterial persistence and might also promote stomach cancer development by allowing transformed cells to escape immune recognition and grow unimpeded to overt malignancy
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