Overstaying their welcome: defective CX3CR1 microglia eyed in macular degeneration.
Age-related macular degeneration (AMD), the most common cause of blindness in the elderly, is characterized by degeneration of the macula and can lead to loss of fine color vision. Alterations in inflammatory and immune system pathways, which arise from genetic differences, predispose individuals to AMD. Yet the mechanism of disease progression with respect to inflammation is not fully understood. In this issue of the JCI, the study by Combadière and colleagues shows that CX3C chemokine receptor 1-deficient (CX3CR1-deficient) mice have abnormal microglia that accumulate beneath the retina and contribute to the progression of AMD.
Chen
Jing
J
Department of Ophthalmology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, USA.
Connor
Kip M
KM
Smith
Lois E H
LE
D000818:Animals; D000073883:CX3C Chemokine Receptor 1; D020022:Genetic Predisposition to Disease; D006801:Humans; D008268:Macular Degeneration / Q000235:genetics* / Q000473:pathology* / Q000628:therapy; D051379:Mice; D017628:Microglia / Q000473:pathology*; D019707:Receptors, Chemokine / Q000235:genetics / Q000502:physiology*; D012160:Retina / Q000473:pathology / Q000503:physiopathology
D000073883:CX3C Chemokine Receptor 1; C095235:CX3CR1 protein, human; D019707:Receptors, Chemokine