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Updated: Dec 16, 2025
Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
Parental Uveitis Influences Offspring With an Increased Susceptibility to the Experimental Autoimmune Uveitis
Guangnian Yin1,2, Wenxin Zeng1,2, Kaijiao Hu1,2
1Laboratory Animal Center, Chongqing Medical University, Chongqing, China.
Insights
Parental uveitis in mice increases offspring susceptibility to experimental autoimmune uveitis (EAU). This may occur by altering immune cell responses and gene expression, leading to earlier onset and more severe disease in offspring.
Area of Science:
- Ophthalmology
- Immunology
- Genetics
Background:
- Parental health conditions like inflammation and obesity can impact offspring development.
- Experimental autoimmune uveitis (EAU) is an autoimmune eye disease with potential genetic and environmental influences.
Purpose of the Study:
- To investigate the impact of parental uveitis on offspring development.
- To assess offspring susceptibility to developing EAU.
Main Methods:
- Parental mice with induced uveitis were mated.
- Offspring underwent gross examination, gene expression profiling of affected eyes, and EAU susceptibility testing.
- Immune responses, including T-cell proliferation and IL-17 production, were analyzed.
Main Results:
- Offspring of uveitic parents exhibited developmental delays and immune system gene expression changes.
- Offspring showed increased susceptibility, earlier onset, and greater severity of EAU.
- Elevated IRBP-specific lymphocyte proliferation and IL-17 production were noted in offspring exposed to parental uveitis.
Conclusions:
- Parental uveitis can predispose offspring to EAU.
- Altered cell adhesion molecules and antigen presentation may mediate this increased susceptibility.
- T-cell proliferation and Th17 responses are likely involved in the pathogenesis of EAU in offspring from affected parents.
Abstract:
Purpose: Previous studies have shown that parental abnormal physiological conditions such as inflammation, stress, and obesity can be transferred to offspring. The purpose of this study was to investigate the impact of parental uveitis on the development and susceptibility to experimental autoimmune uveitis (EAU) in offspring. Methods: Parental male and female B10RIII mice were immunized with interphotoreceptor retinoid binding protein (IRBP) 161-180 in complete Freund's adjuvant and were immediately allowed to mate. Gross examination of the offspring gestated with EAU was performed to determine the influence of parental uveitis on offspring development after birth. Gene expression profiles were analyzed in the affected eyes of offspring under EAU to identify differentially expressed genes (DEGs). Adult offspring were given 5, 25, and 50 μg IRBP161-180 to compare their susceptibility to EAU. Immunized mice were clinically and pathologically evaluated for the development of EAU. Ag-specific T-cell proliferation and IL-17 production from spleens and lymph nodes were evaluated on day 14 or 35 after immunization. Results: Hair loss, delay of eye opening, and swollen spleens in the offspring from parents with uveitis were observed from day 14 to 39 after birth. DEGs were involved in the immune system process, muscle system process, and cell development. The altered antigen processing and presentation, cell adhesion molecules, and phagosome in the eyes of the offspring from uveitis-affected parents were enriched. Offspring gestated with EAU showed a susceptibility to EAU and an earlier onset and higher severity of EAU compared to the control group mice. IRBP-specific lymphocyte proliferation and IL-17 production were observed in the EAU offspring with exposure to parental uveitis. Conclusions: The results suggest that mouse parents with uveitis can increase their offspring's susceptibility to EAU, probably through altering cell adhesion molecules and antigen processing and presentation related to the T-cell proliferation and Th17 response.
