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*
Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan;
Department of Ophthalmology, School of Medicine, Hokkaido University, Sapporo, Japan; and
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-
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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