Scavenger receptors have been identified as cell surface proteins that recognize modified forms of lipoproteins and thereby promote macrophage foam cell formation during atherosclerosis.
1 We now know that scavenger receptors have a broad role in immune cell biology, including macrophage polarization, innate immune signaling, and cytokine production.
2 In this edition of
IOVS,
Jawad and colleagues 3 asked the question whether knockout of the two class A scavenger receptors, SR-A and MARCO, affects chemokine levels, leukocyte infiltration, and CNV formation in the mouse eye. They used laser-induced damage of Bruch's membrane to trigger CNV formation and thereby modeled the major hallmark of wet AMD. Jawad et al. showed that deficiency of SR-A, MARCO, or both markedly diminished the recruitment of macrophages and neutrophils to early laser lesions, resulting in significantly smaller lesion volumes at late-stage CNV. Using temporal expression profiling with DNA microarrays, the authors also identified a reduced global chemokine and chemokine receptor expression in laser-treated scavenger receptor deficient eyes. This recent study clearly suggests that class A scavenger receptors expressed on macrophages promote a proinflammatory environment and contribute to CNV development in the eye. It will be interesting to see whether class A scavenger receptors interact with the complement system, another important component of AMD-related innate immunity. In the future, scavenger receptors may serve as molecular markers for inflammatory macrophages and targets for immunomodulatory therapies in the eye.