What is it about?
In this study we showed that ocular surface inflammation can be elicited by prototype allergen (papain) through the damage of ocular surface epithelium. The damaged ocular surface produce type-2 immunity initiating cytokines (IL-33 and TSLP), which activate innate lymphoid type 2 cells and subsequent type-2 reactions (eosinophil and basophil infiltration), without the involvement of adaptive immunity dependent components.
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Why is it important?
Traditionally, it was thought adaptive immunity dependent mechanism (antigen specific reactions mediated by T cells) play major roles for ocular surface inflammation. In this study, we showed innate immunity-dependent mechanism could elicit ocular surface type 2 inflammation without the involvement of adaptive immunity-dependent components.
Perspectives
Recently, immunosuppressants like tacrolimus or cyclospolin are used for treatments of severe ocular allergic inflammation. They improved the clinical outcomes, however, there are some cases which do not respond immunosuppressants against adaptive immunity. From our results we consider that anti-IL-33/TSLP therapy may be promising as novel anti allergic therapies against refractory ocular allergy.
Akira Matsuda
Gakko Hojin Juntendo
Read the Original
This page is a summary of: Contributions of Interleukin-33 and TSLP in a papain-soaked contact lens-induced mouse conjunctival inflammation model, Immunity Inflammation and Disease, July 2017, Wiley,
DOI: 10.1002/iid3.189.
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