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International Immunology Advance Access originally published online on January 17, 2008
International Immunology 2008 20(3):365-374; doi:10.1093/intimm/dxm148
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© The Author 2008. Published by Oxford University Press on behalf of The Japanese Society for Immunology. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press and The Japanese Society for Immunology are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Antigen-dependent monophasic or recurrent autoimmune uveitis in rats

Maria Diedrichs-Möhring, Christiane Hoffmann and Gerhild Wildner

Section of Immunobiology, Department of Ophthalmology, Ludwig-Maximilians-University, Mathildenstrasse 8, 80336 Munich, Germany

Correspondence to: G. Wildner; E-mail: gerhild.wildner{at}med.uni-muenchen.de

Experimental autoimmune uveitis (EAU) in the Lewis rat has been regarded as an acute and monophasic disease. Uveitis can be induced by immunization with retinal soluble antigen (S-Ag), interphotoreceptor retinoid-binding protein (IRBP) or their peptide derivatives (PDSAg from S-Ag and R14 from IRBP) in CFA as well as by the transfer of activated, antigen-specific T cells. Previously, it has been shown that adoptively transferred, IRBP peptide-specific, but not S-Ag peptide-specific T cells can induce relapsing uveitis in rats. We observed spontaneous recurrences of intra-ocular inflammation even after immunization with R14 in CFA and were able to experimentally re-induce uveitis in rats previously immunized with autoantigen peptide in CFA. The efficiency of re-induction was dependent on the mode of pre-treatment [immunization or adoptive transfer (AT)] as well as on the antigen itself. Primary PDSAg-responses prevented subsequent re-induction of disease much more efficiently than primary R14-mediated EAU. In our model, the suppressive effect of CFA did not play a key role in preventing re-induction or spontaneous relapses. Furthermore, epitope spreading could not be demonstrated as a cause for recurrent inflammation. These data suggest that autoimmune responses with different antigen specificities could underlie similar clinical pictures while being differently regulated, which may help explain the variations in the disease courses in patients and the differential responses to therapeutic modalities.

Keywords: EAU, epitope spreading, experimental re-induction, IRBP, S-Ag

Transmitting editor: T. Hünig

Received 22 May 2007, accepted 13 December 2007.


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