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The anti-inflammatory actions of Developmental Endothelial Locus-1 (Del-1)

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Molecular inhibition of inflammation

Understanding the process of inflammation is central for treating or preventing inflammatory conditions. By focusing on a secreted molecule that blocks inflammation, European researchers provided a novel therapeutic angle.

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During inflammation, leukocytes get recruited to the injured site following a cascade of events that involve activation and migration from the vessels within the endothelium. Several adhesion receptors, including integrins, such as lymphocyte function-associated antigen 1 (LFA-1), promote interactions between leukocytes and the vascular endothelium. Although many adhesion receptors are known to promote leukocyte recruitment, very little information exists about endogenous inhibitors of the cascade. Scientists on the EU-funded project 'The anti-inflammatory actions of developmental endothelial locus-1 (Del-1)' (ANTIINFLDEL) identified the endothelial-derived secreted molecule Del-1 as an endogenous anti-inflammatory agent. This molecule antagonises LFA-1-dependent leukocyte adhesion and recruitment at the site of inflammation. Also, mice lacking Del-1 display a pro-inflammatory phenotype with higher leukocyte recruitment. The scope of ANTIINFLDEL was to delineate the role of Del-1 in inflammation of neuronal organs, such as the retina of the eye. Researchers found that Del-1 is expressed in immune-privileged sites, including the brain and retina, and that expression was abundant in neuronal cells. In addition, induction of inflammation in mice correlated with a reduction in Del-1 levels. Taken together, these observations underscore the homeostatic importance of Del-1 in immune-privileged sites. They also suggest that long-term Del-1 could be exploited therapeutically to reduce the extent of inflammation.


Inflammation, leukocytes, LFA-1, anti-inflammatory, Del-1

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