Abstract
Purpose: The complement system plays important roles in a variety of chronic ocular diseases such as age-related macular degeneration. Here we examined the deposition of complement components in mouse eyes damaged by various mechanisms. Methods: Mouse eyes were damaged by light or by three models of inflammation, i.e., local transgenic expression of cytokines, interleukin-1 or -7, or by induction of experimental autoimmune uveitis. Eye tissues obtained from each model were immunostained with antibodies against complement components C1q, C3, and C4. Results: No complement deposition was seen in light damaged eyes, while in inflamed eyes we found complement deposition at sites of tissue damage and cellular infiltration. In addition to affected tissues, intense immunoreactivity against complement was unexpectedly observed in corneal tissues and lens capsule, despite lack of inflammation in these tissues. Conclusion: Our observations suggest that ocular tissues adjacent to inflammatory sites undergo changes that facilitate complement deposition.
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