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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 mixedcell 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-syndromelike 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. Invest Ophthalmol Vis Sci. 2004; 45: 13751381 ; DOI: 10.1167 iovs.03-0755 toconjunctivitis sicca.1 A combination of immunologic, genetic, hormonal, and environmental factors may play a role in the development of autoimmunity in the lacrimal gland.2, 3 Mononuclear cell infiltration proximal to epithelial cells of the exocrine glands is the typical pathologic finding. The infiltrates consist primarily of CD4 cells. An inflammatory, or Th-1 type, cytokine profile generally has been thought to be characteristic of SjS. There is evidence that the infiltrates produce proinflammatory cytokines, including interleukin IL ; -1, -6, -12, and -18; interferon IFN ; - ; and tumor necrosis factor TNF ; - .4 8 However, in addition to the regulatory cytokines IL-10 and transforming growth factor TGF ; - 1, the Th-2 cytokine IL-4 is detected in some samples, 9 10 where it has been suggested to be associated with B-cell proliferation.11 Moreover, there is evidence that the epithelial cells themselves can significantly influence the overall cytokine profile and the biological consequences of mononuclear cell infiltration.9, 12 Interleukin-10 is a cytokine originally identified as a "cytokine synthesis inhibitory factor" because of its ability to suppress cytokine synthesis in Th1 cells.13 In vitro and in vivo studies show that IL-10 inhibits macrophage monocyte-dependent antigen presentation by downregulating the expression of major histocompatibility complex MHC ; class II, costimulatory molecules CD40, CD80, and CD86 ; , and intercellular adhesion molecule ICAM ; -1. In addition, IL-10 strongly inhibits production of cytokines such as Th1 differentiating cytokine, IL-12 ; and proliferation of CD4 T cells, thereby inducing and maintaining T-cell nonresponsiveness or anergy.14, 15 However, IL-10 also has immunostimulatory properties, especially on CD8 T cells and B cells.14 These pleiotropic effects may explain the discrepancy observed after IL-10 treatment in different in vivo experimental models. Human IL-10 and the vIL-10 encoded by the Epstein-Barr virus have an 84% sequence homology, with most differences occurring in the N-terminal 20 amino acids. The vIL-10 mimics several immunosuppressive activities of human IL-10; however, unlike human IL-10, vIL-10 does not enhance class II MHC expression on mouse B cells, 16 nor does it effectively costimulate mouse thymocyte or mast cell proliferation.17 Interleukin-10 is regarded as a potential therapeutic agent for inflammatory diseases involving Th1 responses because of its ability to downregulate several major functions of Th1 cells and macrophages. Currently, recombinant human IL-10 is being tested in such human autoimmune diseases as rheumatoid arthritis, Crohn's disease, multiple sclerosis, and psoriasis.18, 19 In a previous study, using an adenovirus construct capable of inducing transient vIL-10 gene expression, we demonstrated that lacrimal gland epithelial cells LGECs ; can be transduced in vitro and that detectable, functional vIL-10 suppresses the ability of these cells to activate lymphocytes in autologous mixed-cell reactions.20 More recently, we reported that progressive lacrimal gland dysfunction and ocular surface disease-- characterized by reduced tear production, reduced tear stability, and abnormal staining of the cornea surface, and an increased number of infiltrating CD4 , RTLA , and CD18 cells-- developed in animals whose lacrimal glands were injected with LGEC-stimulated lymphocytes.21 These important 1375.
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Least one dose of study medication 100 to 800 mcg ; . Patients experienced an average of three breakthrough episodes per day. The mean fentanyl effervescent buccal tablet dose was 514.8 mcg per breakthrough episode. Dose adjustments were required by 15.5% of patients, with 2.3% requiring the next lower dose and 10.9% requiring the next higher dose. At the time of the interim analysis, 6% received the 100 mcg dose, 16% were at the 200 mcg dose, 21% were at the 400 mcg dose, 26% were at the 600 mcg dose, and 31% were at the 800 mcg dose. The most common adverse reactions included nausea 35% ; , vomiting 20% ; , dizziness 20% ; , fatigue 15% ; , headache 12% ; , and anemia 11% ; .8, 9, 10 The pooled data from the openlabel, dose-titration phase of three and anacin.
Results Travieso, McRae take hard-fought sprint wins By Matt Krebsbach Frank Travieso AEG-Toshiba-JetNetwork ; won a hard-charging field sprint ahead of Frank Pipp HealthNet Maxxis ; in the men's pro event at the Fourth Annual AT&T Austin Downtown Criterium in Austin, Texas on Saturday. Travieso stormed to the line from inside the pack after it swallowed up early breakaway rider Sean Sullivan Toyota United ; with a mere 300 meters remaining in the race. Sullivan's Toyota United teammate, Serbian national champion Ivan Stevic, took third, behind second placed Frank Pipp Priority Health ; . "I said to myself that I had to do it, " said Travieso. "I Frank Travieso AEG Toshiba ; Photo : Rick Kent attacked on the last lap to get the breakaway. Things were going really fast, but when I go to the last corner I looked back and I had got a real big gap." Travieso had almost become a race casualty when he struck his knee on the top tube of his bike frame as he initiated his effort. "I almost crashed because I took that corner too fast and almost lost my rear wheel, " he explained. "But I got control of my bike, kept my sprint, and made it the whole way." While the Toyota United squad put in its usual strong effort at the front, having only three guys, Sean Sullivan, Ivan Stevic and Henk Vogels, at the event made the task at hand difficult. "We were hoping Sean would make it to the finish, " Stevic said. "It was really hard to control things with only three guys." Fresh off of two wins at the Tulsa Tough Cycling Festival, Austinite Jen McRae Advil-Chapstick ; came good on her billing as the pro women's race favorite. McRae held off Shontell Gauthier Team Ultralink ; and Allyson Brandt HealthCoach ; , to take the women's victory. Throughout the one kilometer circuit, McRae was never far from the front of the field, showing that she's still one of the best female racers in the North America.
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