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KMID : 1225720220140040424
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Allergy, Asthma & Immunology Research : AAIR
2022 Volume.14 No. 4 p.424 ~ p.438
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Interleukin-18 Receptor α Modulates the T Cell Response in Food Allergy
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Kim Eun-Gyul
Leem Ji-Su
Baek Seung-Min
Kim Hye-Rin
Kim Kyung-Won
Kim Mi-Na
Sohn Myung-Hyun
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Abstract
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Purpose: The prevalence of food allergy, triggered by T-helper type 2 (Th2) cell-mediated inflammation, is increasing worldwide. Interleukin (IL)-18 plays an important role in inflammatory diseases by binding with the IL-18 receptor. IL-18/IL-18 receptor α (IL-18Rα) is a cofactor for immunoglobulin E (IgE) production and Th2 cell development. Studies have not investigated the association between the IL-18/IL-18Rα signaling pathway and food allergy. Here, we investigated the role of IL-18Rα in food allergy induction and development.
Methods: Wild-type (WT) and IL-18Rα-null mutant (IL-18Rα?/?) C57BL/6 mice were sensitized and challenged using ovalbumin (OVA) for food allergy induction. Food allergy symptoms, T cell-mediated immune responses, and signal transducer and activator of transcription (STAT)/suppressors of cytokine signaling (SOCS) pathways were analyzed in mice.
Results: IL-18Rα expression was increased in WT mouse intestines after OVA treatment. Food allergy-induced IL-18Rα?/? mice showed attenuated systemic food allergic reactions, OVA-specific IgE and mouse mast cell protease-1 production, inflammatory cell infiltration, and T cell activation. Ex vivo experiments showed that cell proliferation and Th2 cytokine production were lower in IL-18Rα?/? mouse splenocytes than in WT mouse splenocytes. IL-18Rα blockade in WT splenocytes attenuated cell proliferation and Th2 cytokine production. Moreover, STAT3 phosphorylation was reduced in IL-18Rα?/? mice, and SOCS3 and SOCS1 activation were diminished in IL-18Rα?/? intestinal T cells.
Conclusions: IL-18Rα regulates allergic reactions and immune responses by regulating T cell responses in food allergies. Moreover, IL-18Rα is involved in the STAT/SOCS signaling pathways. Targeting IL-18Rα signaling might be a novel therapeutic strategy for food allergy.
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KEYWORD
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Food allergy, interleukin-18, receptors, Th2 cells, STAT3 Transcription Factor, suppressors of cytokine signaling proteins, pathophysiology
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