The anterior chamber of the eye is known to be an immune privileged site, due to both local and systemic effects on the immune response. Injection of IFN-γ into the anterior chamber (AC) overcomes the suppression of antigen-specific delayed hypersensitivity responses normally seen in the eye. Transgenic mice expressing increased IFN-γ in the lens under the αA-crystallin promoter were produced to determine whether the proinflammatory effects of IFN-γ would abolish immune privilege and promote loss of tolerance as has been seen in non-immune privileged tissues. Two αC/IFN-γ transgenic lines are described which demonstrate multiple ocular and lenticular abnormalities some of which are developmental in origin and others that may be secondary to the inflammatory effects of IFN-γ A significant inflammatory cell infiltrate which is observed in the AC and vitreous from birth to 4 weeks of age, consists initially of macrophage and polymorphonuclear leukocytes and then CD4+ T lymphocytes. However, the infiltrate is essentially resolved by 6 weeks of age. Therefore, although lens-specific expression of IFN-γ results in early loss of immune privilege, chronic uveitis does not occur probably due to the lack of continued IFN-γ expression.
|Number of pages||9|
|Journal||Current Eye Research|
|State||Published - 1995|
Bibliographical noteFunding Information:
The authors would like to thank You Xia for her excellent technical help in maintaining and screening the transgenic mice and to Dr Sonya Carlson for her suggestions for immunohistochemistry. The authors also thank Sylvia Valle for histological sections and Mike Green for microinjection and transgenic mouse production. This work was supported by the University of Kentucky Medical Center Research Fund and NIH grant EY09638.
- Ocular inflammation
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience