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Inflammation

The GEF way to MYD88-dependent vascular permeabilization

Nature Reviews Immunology volume 12, page 807 (2012)Cite this article

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The integrity of the vasculature is compromised under inflammatory conditions, partly as a result of low surface levels of the cell–cell adhesion molecule VE-cadherin. Now Zhu et al. delineate the signalling events that lead to vascular permeabilization following the stimulation of human endothelial cells with interleukin-1β (IL-1β). IL-1β induced NF-κB-independent activation of the GTPase ARF6, which promoted the endocytosis of VE-cadherin. The guanine nucleotide-exchange factor (GEF) ARNO was required for ARF6 activation and co-immunoprecipitated with the IL-1β signalling adaptor molecule MYD88. As the GEF inhibitor SecinH3 reduced vascular permeabilization and tissue inflammation in two models of inflammatory disease, specific targeting of this GEF-dependent arm of IL-1β signalling may be of therapeutic value.

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ORIGINAL RESEARCH PAPER

  1. Zhu, W. et al. Interleukin receptor activates a MYD88–ARNO–ARF6 cascade to disrupt vascular stability. Nature 11 Nov 2012 (doi:10.1038/nature11603)

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  1. Maria Papatriantafyllou
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Papatriantafyllou, M. The GEF way to MYD88-dependent vascular permeabilization. Nat Rev Immunol 12, 807 (2012). https://doi.org/10.1038/nri3354

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