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. 2009 Apr 17;5(4):e1000393. doi: 10.1371/journal.ppat.1000393

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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(A) Splenocytes were harvested from mice sufficient (HET, +/−) or deficient (KO, −/−) in Retnla 12 days after i.p. sensitization with 5000 viable S. mansoni eggs. Cells were stimulated with media, SEA (25 µg/ml) or ConA (1 µg/ml) in duplicate for 72 h at 37°C at which time supernatants were harvested and tested for IL-4 by ELISA. (B) Separate groups of SEA stimulated cells were also treated with PBS or rRelma (0.5 µg/ml) and examined for IL-4 (bars show Means±SD). (C) WT C57BL/6, IL-13KO, IFN-γ KO, IL-13/IFN-γKO, IL-4KO, IL-4/IL-13KO, and IL-4/IL-13/IFN-γ KO mice were infected with 30–35 S. mansoni cercariae and liver mRNA was isolated on wk 9 post-infection and prepared individually for real-time RT-PCR analysis of Retnla. Gene expression (mean±SEM) is expressed as the fold-increase over naïve WT controls after normalization to HPRT. The results from individual mice are shown. (D) Model depicting the role of Retnla in the regulation of Th2-driven inflammation, fibrosis and immunity to GI nematode infection. Retnla is induced by IL-4 and IL-13 and inhibits the Th2 effector response.