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2. Self-destructive cooperation mediated by phenotypic noise

3. NADPH oxidase deficient mice develop colitis and bacteremia upon infection with normally avirulent, TTSS-1- and TTSS-2-deficient Salmonella Typhimurium

4. TLR5 signaling stimulates the innate production of IL-17 and IL-22 by CD3negCD127+ immune cells in spleen and mucosa1

5. Salmonella Typhimurium diarrhea as a result of pathogen invasion and immune defence

6. Near surface swimming of Salmonella Typhimurium explains target-site selection and cooperative invasion

7. TLR5 Signaling Stimulates the Innate Production of IL-17 and IL-22 by CD3(neg)CD127(+) Immune Cells in Spleen and Mucosa

8. Near Surface Swimming of Salmonella Typhimurium Explains Target-Site Selection and Cooperative Invasion

9. Salmonella Gut Invasion Involves TTSS-2-Dependent Epithelial Traversal, Basolateral Exit, and Uptake by Epithelium-Sampling Lamina Propria Phagocytes

13. TLR5 Signaling Stimulates the Innate Production of IL-17 and IL-22 by CD3negCD127+ Immune Cells in Spleen and Mucosa

16. NADPH Oxidase Deficient Mice Develop Colitis and Bacteremia upon Infection with Normally Avirulent, TTSS-1- and TTSS-2-Deficient Salmonella Typhimurium.

17. Accelerated Type III Secretion System 2-Dependent Enteropathogenesis by a Salmonella entericaSerovar Enteritidis PT4/6 Strain

18. NADPH Oxidase Deficient Mice Develop Colitis and Bacteremia upon Infection with Normally Avirulent, TTSS-1- and TTSS-2-Deficient Salmonella Typhimurium

19. Stromal IFN-γR-Signaling Modulates Goblet Cell Function During Salmonella Typhimurium Infection

20. IL-17A/F-Signaling Does Not Contribute to the Initial Phase of Mucosal Inflammation Triggered by S. Typhimurium

21. NADPH oxidase deficient mice develop colitis and bacteremia upon infection with normally avirulent, TTSS-1- and TTSS-2-deficient Salmonella Typhimurium.

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