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Volume 23 Issue 5, May 2017

West et al. (p 579), find that the cytokine oncostatin M (OSM) and its receptor are upregulated in the inflamed intestinal tissue from patients with inflammatory bowel disease (IBD). High OSM expression was associated with resistance to tumor necrosis factor (TNF)-neutralizing therapy. OSM blockade or genetic deletion attenuated disease severity in a mouse model of anti-TNF resistant IBD, suggesting that OSM may be a promising therapeutic target. Image depicts inflamed mouse colon mucosa, with an expanded population of intestinal stromal cells identified by expression of podoplanin (green). Epithelium is identified by expression of EpCAM (magenta); cyan, nuclei. Image credit, Samuel Bullers.

Editorial

  • Proposed US budget cuts and the impending exit of the UK from the European Union have the potential to destabilize the global biomedical-research enterprise. In the meantime, the uncertainty of not knowing just how bad the effects will be will inflict its own damage.

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  • A new study identifies oncostatin M (OSM) as a potential biomarker and therapeutic target for anti-tumor necrosis factor (TNF)-refractory inflammatory bowel disease (IBD), and pinpoints mucosal stromal cells as key players in OSM-mediated inflammation.

    • Walter M Kim
    • Arthur Kaser
    • Richard S Blumberg
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    • André M Cantin
    • John W Hanrahan
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  • A recent study using a humanized mouse model shows that HIV-1 can persist in macrophages during antiretroviral therapy (ART), and suggests that macrophages may represent an obstacle to efforts to cure HIV-1 infection.

    • Mario Stevenson
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Perspective

  • In this Perspective, June, Bluestone and Warshauer discuss potential cellular and molecular explanations for the autoimmunity often associated with immunotherapy, and propose additional research and changes to reporting practices to aid efforts to understand and minimize these toxic side effects.

    • Carl H June
    • Jeremy T Warshauer
    • Jeffrey A Bluestone

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