Helicobacter pylori Depletes Cholesterol in Gastric Glands to Prevent Interferon gamma Signaling and Escape the Inflammatory Response

Despite inducing an inflammatory response, Helicobacter pylori can persist in the gastric mucosa for decades. H pylori expression of cholesterol-α-glucosyltransferase (encoded by cgt) is required for gastric colonization and T-cell activation. We investigated how cgt affects gastric epithelial cells and the host immune response.

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