Abstract
A minor haplotype of chromosome 10q26 accounts for much of the genetic risk of age-related macular degeneration (AMD). In this issue of Immunity, Beguier etal. demonstrate that carriers of the 10q26 AMD-risk haplotype overexpress the peptidase HTRA1, which in turns results in mononuclear phagocyte persistence in an immune privileged site and pathogenic inflammation.
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