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. 2014 May 29;5(5):e1269. doi: 10.1038/cddis.2014.218

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Copyright © 2014 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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MST2 promotes inflammatory response after RD. (a and b) ELISA to detect MCP-1 (a) and IL-6 (b) in the WT and MST2^−/− retinas at 24, 48, 72 h after RD (n=8 each). MCP-1 and IL-6 generation at 24 h after RD was suppressed in MST2^−/− mice (*P<0.05). After day 1, MCP-1 and IL-6 levels were decreased in both groups. (c and d) Immunofluorescence for CD11b (c) and time course of CD11b-positive cell density (d) in WT and MST2^−/− mice (n=6 each group and time point). Infiltration of CD11b-positive cells was substantially decreased in MST2^−/− mice at 24 h after RD (**P<0.01). WT mice kept the CD11b-positive cell density after day 1, whereas that in MST2^−/− mice was increased to the same level as WT mice 3 days after RD. The graphs show mean±S.E.M.