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PURPOSE. To evaluate the effect of viral IL-10 on the lacrimal gland immunopathologic response in the ocular surface disease, induced autoimmune dacryoadenitis. METHODS. Disease was induced in rabbits by injecting inferior lacrimal glands with peripheral blood lymphocytes activated by 5 days of coculture with autologous acinar cells in a mixed-cell reaction. In the treated group, an adenoviral vector carrying the vIL-10 gene was concurrently injected with activated lymphocytes. Tears were collected periodically for quantitation of IL-10 by ELISA. Two weeks after disease induction, tear production, tear film breakup time, and rose bengal staining score were determined. Sectioned glands were immunostained for expression of CD4, CD8, rabbit thymic lymphocyte antigen (RTLA), CD18 and major histocompatibility complex class II. RESULTS. The titer of vIL-10 in tears was at its maximum on day 3, started to decline by day 7, and was undetectable by day 14. In the diseased group, the tear production rate and tear film breakup time were significantly decreased, and rose bengal staining was significantly increased. Diseased glands had immune cell infiltrates containing CD4 + , RTLA + , and CD18 + cells, and major histocompatibility complex class II expression was increased. These changes were significantly ameliorated by expression of vIL-10. CONCLUSIONS. In vivo transduction of the lacrimal gland with AdvIL-10 resulted in the transient appearance of VIL-10 in tears. The presence of vIL-10 partially suppressed the appearance of Sjogren-syndrome-like features of reduced tear production, accelerated tear breakup, ocular surface disease, and immunopathologic response. Anti-inflammatory cytokine gene expression may offer a therapeutic modality for the treatment of autoimmune dacryoadenitis, once suitable vectors become available.

The purpose of this study was to evaluate primary afferent visual pathway function by objectively testing contrast sensitivity in persons with Alzheimer's dementia (AD), using a sweep visual evoked potential technique.Twenty-five patients, 16 with AD and 9 elderly control (EC) subjects, were enrolled from the University of Southern California Rancho Los Amigos Medical Center. The patients with AD had clinical dementia ratings ranging from 0.5 to 3, corresponding to mild to moderate disease. All participants underwent refraction and screening for ophthalmic disease. Subjects were evaluated with the sweep visual evoked potential technique. Each trial consisted of logarithmically increasing contrast over a 10-second period. Subjects were evaluated monocularly at spatial frequencies of 1, 5, and 8 cyc/deg. Patients were not required to integrate and respond to stimuli.Mean contrast sensitivity thresholds were significantly higher in patients with AD than in EC subjects. The mean contrast sensitivities in the AD group were 4.0%, 9.6%, and 18.6%, at 1, 5, and 8 cyc/deg, respectively. The corresponding sensitivities in the EC group were 2.1%, 5.3%, and 11.4%, at 1, 5, and 8 cyc/deg, respectively. These threshold differences were significant at probabilities of 0.01, 0.05, and 0.07. There was no correlation between clinical dementia ratings and reduction of contrast sensitivity thresholds. Confounding factors such as age, gender, nuclear sclerosis, and visual acuity were evaluated. Visual acuity was the only factor significantly different between AD responders and AD nonresponders at 1 and 5 cyc/deg.These results suggest patients with AD have deficits in contrast sensitivity attributable to dysfunction of the primary afferent visual pathway.