AI Article Synopsis
- Scientists found a new helper protein called Coro1A that helps white blood cells, called PMNs, attach and move during inflammation.
- Coro1A works with special proteins (β integrins) to make sure PMNs can stick to blood vessel walls and travel where they are needed.
- Mice without Coro1A had a harder time getting PMNs to areas of infection, which means Coro1A is really important for our immune system to work properly.
Article Abstract
Trafficking of polymorphonuclear neutrophils (PMNs) during inflammation critically depends on the β integrins lymphocyte function-associated antigen 1 (LFA-1) (CD11a/CD18) and macrophage-1 antigen (CD11b/CD18). Here, we identify coronin 1A (Coro1A) as a novel regulator of β integrins that interacts with the cytoplasmic tail of CD18 and is crucial for induction of PMN adhesion and postadhesion events, including adhesion strengthening, spreading, and migration under flow conditions. Transition of PMN rolling to firm adhesion critically depends on Coro1A by regulating the accumulation of high-affinity LFA-1 in focal zones of adherent cells. Defective integrin affinity regulation in the genetic absence of impairs leukocyte adhesion and extravasation in inflamed cremaster muscle venules in comparison with control animals. In a mouse infection model, PMN infiltration into the gastric mucosa is dramatically reduced in mice, resulting in an attenuated gastric inflammation. Thus, Coro1A represents an important novel player in integrin biology, with key functions in PMN trafficking during innate immunity.
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| http://dx.doi.org/10.1182/blood-2016-11-749622 | DOI Listing |
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