Spontaneous retinopathy in HLA-A29 transgenic mice
- Yann Szpak†,
- Jean-Claude Vieville†,
- Thierry Tabary‡,
- Marie-Christine Naud§,
- Martine Chopin†,
- Catherine Edelson‡,
- Jacques H. M. Cohen‡,
- Jean Dausset¶,
- Yvonne de Kozak§, and
- Marika Pla†,‖
- †Mouse Immunogenetics, Institut National de la Santé et de la Recherche Médicale, Unité 462, Institute of Hematology, Saint-Louis Hospital, 1 Avenue Claude Vellefaux, 75475 Paris Cedex 10, France; ‡Laboratoire d'Immunologie, Unité de Formation et de Recherche Médecine, Physio-Pathologie Dys-Immunitaire Humaine, EA 000 Pole Biomolécules IFR 53, Université de Reims Champagne-Ardennes, 51100 Reims, France; §Development, Aging, and Pathology of the Retina, Institut National de la Santé et de la Recherche Médicale, Unité 450, Centre Biomédical des Cordeliers, 15 Rue de l'Ecole de Médecine, 75006 Paris, France; and ¶Human Polymorphism Study Center, 27 Rue Juliette Dodu, 75010 Paris, France
-
Contributed by Jean Dausset
Abstract
Humans who have inherited the class I major histocompatibility allele HLA-A29 have a markedly increased relative risk of developing the eye disease termed birdshot chorioretinopathy. This disease affecting adults is characterized by symmetrically scattered, small, cream-colored spots in the fundus associated with retinal vasculopathy and inflammatory signs causing damage to the ocular structures, leading regularly to visual loss. To investigate the role of HLA-A29 in this disease, we introduced the HLA-A29 gene into mice. Aging HLA-A29 transgenic mice spontaneously developed retinopathy, showing a striking resemblance to the HLA-A29-associated chorioretinopathy. These results strongly suggest that HLA-A29 is involved in the pathogenesis of this disease. Elucidation of the role of HLA-A29 should be assisted by this transgenic model.
Footnotes
-
↵ ‖ To whom reprint requests should be addressed. E-mail: marika.pla{at}chu-stlouis.fr.
- Abbreviation:
- BSCR,
- birdshot chorioretinopathy
- Copyright © 2001, The National Academy of Sciences
