In:
Ophthalmic Research, S. Karger AG, Vol. 40, No. 3-4 ( 2008), p. 175-180
Abstract:
〈 i 〉 Purpose: 〈 /i 〉 A major increased risk of developing birdshot chorioretinopathy is reported in humans who are HLA-A29-positive. To better characterize this disease, an animal model of HLA-A29-associated disease was developed and the pathology arising spontaneously in these transgenic mice was compared to animal models of autoimmune uveoretinitis and to human pathology. 〈 i 〉 Materials and Methods: 〈 /i 〉 HLA-A2902 cDNA (A29c) was obtained from a patient suffering from birdshot retinochoroidopathy and used for transgene construct to generate HLA-A29 transgenic mice. Histopathological examination of the animal cohort was performed up to 15 months of age. It was compared with the ocular pathology developed in C57BL/6 mice and in Lewis rats immunized with retinal autoantigens. 〈 i 〉 Results: 〈 /i 〉 Aging HLA-A29 transgenic mice spontaneously developed an ocular disease with resemblance to experimental retinal-Ag-induced autoimmune ocular disease and to human pathologies shown in birdshot retinochoroidopathy, Vogt-Koyanagi-Harada and sympathetic ophthalmia. Pathogenic mechanisms could possibly be shared by these conditions. 〈 i 〉 Conclusion: 〈 /i 〉 Humanized models of ocular inflammation developed in HLA class I and class II transgenic mice will help better understand the mechanisms responsible for ocular inflammation. Local control of autoimmunity in HLA-A29-positive individuals would be an important option for new therapeutic strategies.
Type of Medium:
Online Resource
ISSN:
0030-3747
,
1423-0259
Language:
English
Publisher:
S. Karger AG
Publication Date:
2008
detail.hit.zdb_id:
1483177-6
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