These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Transgenic mice expressing IFN-gamma in the retina develop inflammation of the eye and photoreceptor loss. Author: Geiger K, Howes E, Gallina M, Huang XJ, Travis GH, Sarvetnick N. Journal: Invest Ophthalmol Vis Sci; 1994 May; 35(6):2667-81. PubMed ID: 8188461. Abstract: PURPOSE: Inflammatory mediators such as interferon-gamma (IFN-gamma) are thought to play a role in ocular disease. Although IFN-gamma was found in the vitreous of mice with experimentally induced autoimmune uveitis, intracameral injection of this cytokine did not induce intraocular inflammation in mice. Therefore, the authors created a transgenic mouse line using the rhodopsin promoter to direct the expression of IFN-gamma in the photoreceptor cells of the retina. These mice, designated rho gamma, enabled them to model intraocular inflammatory disease. METHODS: The authors fused a 2.1 kb 5' Hind III fragment from the murine rhodopsin gene to the IFN-gamma gene and introduced the DNA construct into fertilized zygotes. These were implanted into pseudopregnant C57BL/6 mice, and the resulting progeny were crossed back to balb/c mice. The transgene was identified by Southern blot hybridization. Eyes from the rho gamma mice were either fixed in zinc formalin and stained with hematoxylin and eosin or were frozen in OCT compound and processed for immunostaining using the indirect immunoperoxidase method with DAB as a chromogen. RESULTS: The rho gamma transgenic mice developed intraocular disease, manifested as intraocular cellular infiltration, loss of photoreceptors, corneal clouding, cataract formation, and epithelial and microglial proliferation. Additionally, rho gamma mice exhibited antigenic changes, comprising GFAP expression on Müller cells, accumulation of neurofilament on photoreceptors, and expression of MHC class I and class II molecules on retinal cells. CONCLUSIONS: IFN-gamma alters the antigenic properties of intraocular tissue and induces intraocular inflammation in mice. The results suggest a key position of IFN-gamma in the development of pathologic conditions related to intraocular inflammation and provide a useful animal model for the further study of inflammatory disorders, including autoimmune diseases.[Abstract] [Full Text] [Related] [New Search]