Aim: To investigate the involvement of interleukin (IL)10 and transforming growth factor (TGF) β 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 μg of anti-IL10 or anti-TGF β antibodies at 0, 2, 4, 6 and 8 days (induction phase treatment) or 500 μg 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 β 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 β antibody, but not the anti-IL10 antibody, markedly up regulated proliferation and Th2 cytokine production by splenocytes. IL1α levels in the conjunctiva were reduced after treatment with either antibody; in addition, eotaxin and tumour necrosis factor α levels were reduced after treatment with antibody to TGF β.
Conclusions: IL10 and TGF β 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.
- nrIgG, normal rat immunoglobulin G
- PBS, phosphate-buffered saline
- TNF, tumour necrosis factor
- TGF, transforming growth factor
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