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The Journal of Immunology, 00, 165: 2962-2969.
Copyright © 00 by The American Association of Immunologists

Amelioration of Experimental Autoimmune Uveoretinitis by Pretreatment with a Pathogenic Peptide in Liposome and Anti-CD40 Ligand Monoclonal Antibody1

Kenichi Namba*,{dagger}, Kazumasa Ogasawara2,*, Nobuyoshi Kitaichi*,{dagger}, Taiki Morohashi*, Yoichi Sasamoto{dagger}, Satoshi Kotake{dagger}, Hidehiko Matsuda{dagger}, Kazuya Iwabuchi*, Chikako Iwabuchi*, Shigeaki Ohno{ddagger} and Kazunori Onoé3,*

* Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan; {dagger} Department of Ophthalmology, School of Medicine, Hokkaido University, Sapporo, Japan; and {ddagger} Department of Ophthalmology, Yokohama City University School of Medicine, Yokohama, Japan

We have defined a peptide K2 (ADKDVVVLTSSRTGGV) that corresponds to residues 201–216 of bovine interphotoreceptor retinoid-binding protein and induces experimental autoimmune uveoretinitis (EAU)4 in H-2Ak-carrying mice (H-2Ak mice). In this study, we attempted to ameliorate EAU in the H-2Ak mice without nonspecific suppression of T cell responses. Preceding s.c. administration of liposomes including K2 (liposomal K2) specifically inhibited subsequent generation of T cell response to K2. The same result was obtained with a combination of OVA323–339 peptide and the OVA-specific TCR-transgenic T cells. It was suggested that the inhibition was mainly attributed to peripheral anergy induction of T cells specific for the peptide Ag, although specific cell death might also be involved in the inhibition. Pretreatment with liposomal K2 also considerably abolished IFN-{gamma} production but not IL-4 production. The specific inhibitory effect of the pretreatment with liposomal peptide was augmented by a simultaneous administration of anti-CD40 ligand (anti-CD40L) mAb. Moreover, it was shown that the pretreatment with liposomal K2 reduced both the incidence and severity of the subsequent K2-induced EAU, and the simultaneous administration of anti-CD40L mAb augmented this preventive effect by liposomal K2. Our findings demonstrate that the s.c. administration of liposomal pathogenic peptide and anti-CD40L mAb can be applied to preventing autoimmune diseases without detrimental nonspecific suppression of T cell responses.




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