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17 results on '"Bentley JK"'

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1. Tuft cells are required for a rhinovirus-induced asthma phenotype in immature mice.

2. Modeling Asthma in Mice Using Rhinovirus Infection.

3. Deficient inflammasome activation permits an exaggerated asthma phenotype in rhinovirus C-infected immature mice.

4. Rhinovirus C Infection Induces Type 2 Innate Lymphoid Cell Expansion and Eosinophilic Airway Inflammation.

5. Early-life heterologous rhinovirus infections induce an exaggerated asthma-like phenotype.

6. Myristoylated rhinovirus VP4 protein activates TLR2-dependent proinflammatory gene expression.

7. Enterovirus D68 infection induces IL-17-dependent neutrophilic airway inflammation and hyperresponsiveness.

8. IFN-γ Blocks Development of an Asthma Phenotype in Rhinovirus-Infected Baby Mice by Inhibiting Type 2 Innate Lymphoid Cells.

9. Toll-like receptor 2-expressing macrophages are required and sufficient for rhinovirus-induced airway inflammation.

10. Rhinovirus infection induces interleukin-13 production from CD11b-positive, M2-polarized exudative macrophages.

11. Macrophage activation state determines the response to rhinovirus infection in a mouse model of allergic asthma.

13. Airway smooth muscle hyperplasia and hypertrophy correlate with glycogen synthase kinase-3(beta) phosphorylation in a mouse model of asthma.

14. Human rhinovirus 1B exposure induces phosphatidylinositol 3-kinase-dependent airway inflammation in mice.

15. Inhibition of glycogen synthase kinase-3beta is sufficient for airway smooth muscle hypertrophy.

16. Airway smooth muscle growth in asthma: proliferation, hypertrophy, and migration.

17. Modeling Asthma in Mice Using Rhinovirus Infection

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