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Suggested model for the role of IFN-I on monocyte and neutrophil regulation.

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posted on 24.02.2011 by Sang-Uk Seo, Hyung-Joon Kwon, Hyun-Jeong Ko, Young-Ho Byun, Baik Lin Seong, Satoshi Uematsu, Shizuo Akira, Mi-Na Kweon

After influenza infection, hematopoietic stem cell differentiation might be triggered by IFN-I and then MCP-1-producing Ly6Chi monocytes are recruited to the lung. In the absence of IFN-I signaling, Ly6Cint monocytes are alternatively generated and produce KC, which might in turn aggravates lung pathology by attracting excess neutrophils to lung.

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