Phosphatidylserine (PS) is crucial for normal brain activities and functions. The phosphatidylserine (PS) receptor (PSR) might act as a 'tickle' receptor for uptake of apoptotic cells and phosphatidylserine -expressing cell vesicles or blebs. It is also suggested to provide anti-inflammatory and anti-immunity signals, in part resulting from production of transforming growth factor-beta (TGF-beta).
However, the PSR seems to be extremely sensitive to proteolysis by the serine protease, neutrophil elastase. This enzyme would be expected early in acute, neutrophil-dependent inflammatory reactions, and might therefore cause a temporary blockade of the anti-inflammatory consequences of PSR ligation.
As the local vascular permeability increases (seen in most acute inflammation), if plasma inhibitors of the elastase (for example, alpha1-antiprotease) gain access to the tissues, the proteases would be inactivated, allowing replenishment and signalling of the PSR to initiate resolution of the inflammation. The concept places importance on the protease/anti protease balance in the tissues in determining the outcome of inflammatory reactions.
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