These observations underline the importance of protein leakage through a damaged blood-ocular barrier and of direct contact of monocytes/macrophages with RPE cells, as well as their reciprocal potentiating effect on RPE cell proliferation. Thus, early stabilization of the blood-ocular barrier, which would preclude or reduce protein leakage and invasion of inflammatory cells into the eye, could be a target for pharmacologic prevention of PVR.
Vitreous exerts a regulatory effect on monocyte activation and maturation by its content of TGF-beta and possibly hyaluronic acid and may, thus, modify the inflammatory or immune response in the eye.
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