Interleukin 10 and transforming growth factor β contribute to the development of experimentally induced allergic conjunctivitis in mice during the effector phase
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Fukushima, A.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Fukushima, A.
Sumi, T.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Sumi, T.
Fukuda, K.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Fukuda, K.
Kumagai, N.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Kumagai, N.
Nishida, T.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Nishida, T.
Yagita, H.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Yagita, H.
Ueno, H.
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机构:Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Ueno, H.
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[1] Kochi Med Sch, Dept Ophthalmol & Visual Sci, Nankoku, Kochi 7838505, Japan
Aim: To investigate the involvement of interleukin (IL)10 and transforming growth factor (TGF) beta in the development of experimentally induced allergic conjunctivitis in mice. Methods: Balb/c mice were actively sensitised with ragweed in alum, and then challenged with ragweed in eye drops after 10 days. 24 h later, the conjunctivas, spleens and blood were collected for histological and cytokine expression analyses, proliferation and cytokine production assays and measurement of immunoglobulin (Ig) levels. Mice developing experimentally induced allergic conjunctivitis were injected intraperitoneally with 200 mu g of anti-IL10 or anti-TGF beta antibodies at 0, 2, 4, 6 and 8 days (induction phase treatment) or 500 mu g of antibodies 2 h before ragweed challenge (effector phase treatment). Normal rat IgG was used for control injections. Results: Treatment with either anti-IL10 or anti-TGF beta antibodies during the induction phase did not affect eosinophil infiltration into the conjunctiva. By contrast, treatment with either antibody during the effector phase suppressed infiltration. During the effector phase, treatment with anti-TGF beta antibody, but not the anti-IL10 antibody, markedly up regulated proliferation and Th2 cytokine production by splenocytes. IL1 alpha levels in the conjunctiva were reduced after treatment with either antibody; in addition, eotaxin and tumour necrosis factor alpha levels were reduced after treatment with antibody to TGF beta. Conclusions: IL10 and TGF beta do not have immunosuppressive roles in the development of experimentally induced allergic conjunctivitis. Rather, they augment the infiltration of eosinophils into the conjunctiva during the effector phase of experimentally induced allergic conjunctivitis.