Abstract
and found that parietal cells in the infected stomach expressed IFNα/β protein in response to Helicobacter infection and that gastric IFNβ mRNA peaked 2 months after the infection while IFNα and IRF7 expression peaked at 2 to 4 months, followed by the peak in Slfn4 mRNA. Ex vivo IFNα11 (800U/ml) treatment of cultured peritoneal myeloid cells induced a phenotypic shift from Gr1-/Slfn4to Gr1+/Slfn4+ cells correlating with a robust increase in Slfn4 expression in vivo. Conclusion: Hedgehog signaling synergizes with Helicobacter infection to induce acquisition of Slfn4+ MDSCs in the stomach.
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