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J Sakai

Publications and source records attributed to J Sakai.

At least 145 records · Page 8Linked to original sources
PubMed1983

Pharmacological modulation of IgE-dependent mast cell degranulation in experimental autoimmune uveoretinitis.

Immediate hypersensitivity phenomena have been shown previously to occur at the beginning of experimental autoimmune uveoretinitis (EAU) induced in Lewis rats by immunization with purified S-antigen from bovine retina. The onset time and severity of the disease were modified by modulating the mast cell (MC) function. Drugs blocking the release of mediators from MC, disodium cromoglycate and ketotifen, given as eyedrops, slightly delayed the onset and decreased the severity of inflammation. Compound 48/80, a drug effective in depleting MC of their inflammatory mediators, delayed significantly the onset, decreased and sometimes suppressed EAU, when given by the subconjunctival or intraperitoneal routes. No modification of the IgG and the IgE circulating anti-S-antibody level was demonstrated in both types of treatment, whereas in vitro reagin-dependent degranulation of peritoneal MC in the presence of the antigen was decreased in both cases. Identification of MC-bound reagins as IgE was strongly suggested by the blocking effect of anti-IgE antibodies on MC degranulation. These data confirm the link between MC activation and the onset and severity of EAU.

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PubMed1981

S antigen-induced experimental autoimmune uveo-retinitis in rats.

Experimental autoimmune uveoretinitis was induced in rats after one injection of purified retinal S antigen mixed with adjuvants. Lewis and PVG/c rat strains were highly sensitive. S antigens isolated from bovine, human, swine and guinea pig retinas had a high pathogenicity in Lewis rats, whereas allogenic S antigen did not induce the disease. Mycobacterial adjuvant was effect in both disease and antibody production but H. pertussis adjuvant strongly increased the severity of the ocular reaction, giving a hyperacute Arthus-type inflammation, even with low doses of antigen. No disease was found after immunization without bacteria (incomplete Freund's adjuvant or alum). With any bacterial adjuvant, the histological pattern was in agreement with the hypothesis of early reagin-mediated phenomena acting on the blood-retinal barrier, as suggested by previous experiments.

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PubMedDate not supplied

Differentiation of Th1 and Th2 cells in lymph nodes and spleens of mice during experimental autoimmune uveoretinitis.

PURPOSE: Experimental autoimmune uveoretinitis (EAU) is a T-cell-mediated autoimmune disease that can be elicited in susceptible rodent strains by immunization with a retinal autoantigen, such as interphotoreceptor retinoid-binding protein (IRBP). In this study, we investigated whether there is a correlation between inflammation in the eye and T-helper (Th)1- and Th2-type responses in the lymph nodes and the spleen after immunization of B10.A mice with IRBP. METHODS: B10.A mice were immunized with IRBP emulsified with complete Freund's adjuvant (CFA), and eyes were then enucleated for histological examination of EAU at 1, 2, 4, 6, or 8 weeks after immunization. In addition, lymph node cells and spleen cells were collected, and cultured with IRBP to measure T-cell proliferation responses and Th1-type (interleukin [IL]-2, interferon [IFN]-gamma), Th2-type (IL-4, IL-10) cytokine production. RESULTS: Pathologically, severe ocular inflammation occurred 2 weeks after IRBP immunization, persisted for 2 weeks, and then gradually resolved. Interleukin-2 and IFN-gamma production were observed in draining lymph node cells at 1 and 2 weeks after IRBP immunization. Those responses then diminished, whereas IFN-gamma production by spleen cells was observed from week 1, peaked at week 4, and gradually decreased. Alternatively, significant production of IL-4 or IL-10 by draining lymph node cells was not detected at any time point. Both IL-4 and IL-10 production by spleen cells was observed at week 6. CONCLUSIONS: Th1-type responses were observed early in draining lymph nodes, then in the spleen after IRBP immunization. The levels of IFN-gamma production by spleen cells reflected the severity of EAU, confirming their pathogenic role in this disease. Th2-type responses were generated in the spleen only as the disease receded, suggesting a role for Th2 cells in the spontaneous termination of EAU.

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