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G. Wildner, C. Sieg, M. Diedrichs-Möhring, D. Voehringer; Nippostrongylus Brasiliensis Infection in Experimental Autoimmune Uveitis (EAU) of Lewis Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4823.
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© ARVO (1962-2015); The Authors (2016-present)
In the Lewis rat model of EAU the autoimmune response to ocular antigens is mediated by Th1 and Th17 cells. Here we investigated the effect of infection with the nematode N. brasiliensis, a strong inducer of Th2 responses, on EAU induced with retinal S-Antigen peptide PDSAg or IRBP peptide R14. PDSAg induces monophasic disease, while R14 causes relapses.
Seven days post infection with N. brasiliensis larvae the rats were immunized with PDSAg or R14 in CFA to induce EAU or to generate T cell lines. Uveitis intensity was determined clinically and histologically. T cell lines were established from lymph node cells stimulated with the respective antigens. Proliferation was measured and culture supernatants were collected daily and pooled for multiplex cytokine/chemokine analysis.
T cell lines secreted high amounts of IFN-gamma as well as IL-17, irrespective of prior infection of the donor rats with N. brasiliensis or not, and irrespective of the course of disease. The cytokine pattern of T cell lines from non-infected rats with or without recurrent disease was identical. Th2-specific cytokines could not be detected in supernatants of any T cell line, not even from N. brasiliensis-infected rats. Uveitis intensity was not significantly different in infected vs. non-infected rats. However, N. brasiliensis infection abrogated recurrences of EAU after R14-immunization, while 75% of rats from the non-infected control group had relapsing disease.
Both, Th1 as well as Th17 responses are induced in rat EAU, irrespective of the antigen specificity and whether they were infected with N. brasiliensis or not. Infected Lewis rats did not generate a Th2 response protecting from EAU. However, recurrent disease after immunization with IRBP peptide was suppressed in animals with prior infection, while antigen-specific T cells from these animals showed a Th1/Th17 pattern, but no Th2. Neither Th1 nor Th17 cells seem to be crucial for preventing or promoting recurrent EAU in Lewis rats.
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