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Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
Antigen-dependent monophasic or recurrent autoimmune uveitis in rats
Maria Diedrichs-Möhring1, Christiane Hoffmann, Gerhild Wildner
1Section of Immunobiology, Department of Ophthalmology, Ludwig-Maximilians-University, Mathildenstrasse 8, 80336 Munich, Germany.
International Immunology
|January 22, 2008
Summary
Experimental autoimmune uveitis (EAU) can relapse, challenging its monophasic view. Autoimmune responses vary in regulation, explaining diverse disease courses and treatment responses in patients.
Area of Science:
- Ophthalmology
- Immunology
- Autoimmunity
Background:
- Experimental autoimmune uveitis (EAU) in Lewis rats is typically acute and monophasic.
- Uveitis can be induced by retinal antigens (S-Ag, IRBP) or their peptides, via immunization or T-cell transfer.
- Previous studies indicated only IRBP peptide-specific T cells induce relapsing uveitis.
Purpose of the Study:
- To investigate spontaneous recurrences and experimental re-induction of EAU.
- To determine the influence of antigen specificity and pre-treatment on disease recurrence.
- To explore the role of CFA and epitope spreading in EAU relapses.
Main Methods:
- Immunization of Lewis rats with retinal soluble antigen (S-Ag) or interphotoreceptor retinoid-binding protein (IRBP) peptides in Complete Freund's Adjuvant (CFA).
- Adoptive transfer (AT) of antigen-specific T cells.
- Experimental re-induction of EAU in previously immunized rats.
- Assessment of spontaneous recurrences and epitope spreading.
Main Results:
- Spontaneous recurrences of intra-ocular inflammation were observed after R14 immunization.
- EAU could be experimentally re-induced in rats previously immunized with autoantigen peptide.
- Re-induction efficiency depended on pre-treatment method and antigen; PDSAg responses were more suppressive than R14.
- Complete Freund's Adjuvant (CFA) did not significantly prevent re-induction or relapses.
- Epitope spreading was not a cause of recurrent inflammation.
Conclusions:
- Autoimmune responses with distinct antigen specificities can present similarly but are regulated differently.
- Differential regulation of autoimmune responses may explain variations in EAU disease courses.
- Understanding these differences is crucial for explaining patient variability and differential therapeutic responses.
