Experimental autoimmune posterior uveitis accompanied by epitheloid cell accumulations (EAPU). A new type of experimental ocular disease induced by immunization with PEP-65, a pigment epithelial polypeptide preparation.

Purified retinal pigment epithelial cells of bovine eyes have been fractionated by a series of buffer and detergent extractions. The electropherogram of the buffer-insoluble, Triton X-100-soluble fraction (RPE-TS) exhibits a major polypeptide band of M(r) 65 kDa and a variety of minor components. Electrophoretically purified 65 kDa-band protein (PEP-65) is immunologically unrelated to the known uveitogenic photoreceptor proteins, to other neural retina proteins, and to PEP-X, the RPE-melanin-bound uveitogenic antigen. An immunocytochemical study of eye tissues suggests that it is exclusively located in the RPE. Immunization of Lewis rats with PEP-65 or affinity-purified RPE-TS induces a new type of ocular disease: experimental autoimmune posterior uveitis accompanied by epitheloid cell accumulations (monocytes) adjacent to the RPE (EAPU). The disease starts 9 days after immunization, provided that pertussis toxin is used as co-adjuvant. The first clinical signs are transient flare and cells in the anterior chamber. Choroiditis develops, and epitheloid cells accumulate focally along one or both sides of the Bruch's membrane-RPE layer. Such foci resemble, in some respects, Dálen-Fuchs nodules which occur in human sympathetic ophthalmia. Areas of inflammation are frequently localized in the chorioretinal periphery adjacent to the pars plana. Vitreous cell infiltration is the most prominent clinical feature of EAPU. During at least 2 months, extending chorioretinal areas containing epitheloid cell collections remain while the adjacent photoreceptor cells sometimes disappear without being invaded by these cells. Retinal vasculitis is seldomly observed and pinealitis is absent. EAPU has the latter feature in common with PEP-X-induced experimental autoimmune anterior uveitis (EAAU). The two diseases differ from the various photoreceptor antigen-induced forms of EAU where pinealitis and inflammation of the neural retina are prominent features. However, just as in EAU and EAAU, EAPU can be adoptively transferred, and is inhibited by cyclosporin treatment suggesting T-cell dependency.