IL-33, but Not IL-25, Is Crucial for the Development of House Dust Mite Antigen-Induced Allergic Rhinitis

Nakanishi, Wataru; Yamaguchi, Sachiko; Matsuda, Akira; Suzukawa, Maho; Shibui, Akiko; Nambu, Aya; Kondo, Kenji; Suto, Hajime; Saito, Hirohisa; Matsumoto, Kenji; Yamasoba, Tatsuya; Nakae, Susumu

doi:10.1371/journal.pone.0078099

Cited by 55 publications

(49 citation statements)

References 31 publications

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“…Although epithelial barrier tissues and endothelial cells are generally known to express IL-33 (36,37), some immune cells, such as macrophages and dendritic cells, can produce IL-33 under certain inflammatory conditions (38,39). However, the level of IL-33 produced by hematopoietic cells is much less than that from epithelial cells (39,40), and tissuederived IL-33 is critical for induction of allergic inflammation (41). IL-33 signals through the ST2/IL-1RAcP complex, mainly expressed in ILC2, mast cells, basophils, eosinophils, Th2 cells, NKT, and NK cells (25,42,43).…”

Section: Discussionmentioning

confidence: 99%

Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa

Kim

Chang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Commensal microbiota are well known to play an important role in antiviral immunity by providing immune inductive signals; however, the consequence of dysbiosis on antiviral immunity remains unclear. We demonstrate that dysbiosis caused by oral antibiotic treatment directly impairs antiviral immunity following viral infection of the vaginal mucosa. Antibiotic-treated mice succumbed to mucosal herpes simplex virus type 2 infection more rapidly than water-fed mice, and also showed delayed viral clearance at the site of infection. However, innate immune responses, including type I IFN and proinflammatory cytokine production at infection sites, as well as induction of virusspecific CD4 and CD8 T-cell responses in draining lymph nodes, were not impaired in antibiotic-treated mice. By screening the factors controlling antiviral immunity, we found that IL-33, an alarmin released in response to tissue damage, was secreted from vaginal epithelium after the depletion of commensal microbiota. This cytokine suppresses local antiviral immunity by blocking the migration of effector T cells to the vaginal tissue, thereby inhibiting the production of IFN-γ, a critical cytokine for antiviral defense, at local infection sites. These findings provide insight into the mechanisms of homeostasis maintained by commensal bacteria, and reveal a deleterious consequence of dysbiosis in antiviral immune defense.commensal microbiota | dysbiosis | IL-33 | herpes simplex virus type 2 | genital tract

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Section: Discussionmentioning

confidence: 99%

Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa

Kim

Chang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…IL-33 plays a role in other models of allergic disease, including allergic rhinitis and chronic rhinosinusitus through activation of ILC2s, basophils and mast cells (Haenuki et al, 2012; Kato, 2015; Mjösberg et al, 2011; Nakanishi et al, 2013). In humans, chronic eosinophilic rhinosinusitis with nasal polyps is associated with increased epithelial IL-33 and IL-13 + ILC2s (Shaw et al, 2013).…”

Section: Il-33 In Type 2 Immune Responsesmentioning

confidence: 99%

Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation

2015

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Summary Interleukin-33 (IL-33) is a nuclear-associated cytokine of the IL-1 family originally described as a potent inducer of allergic type 2 immunity. IL-33 signals via the receptor ST2, which is highly expressed on group 2 innate lymphoid cells (ILC2s) and T helper 2 (Th2) cells, thus underpinning its association with helminth infection and allergic pathology. Recent studies have revealed ST2 expression on subsets of regulatory T cells, and for a role for IL-33 in tissue homeostasis and repair that suggests previously unrecognized interactions within these cellular networks. IL-33 can participate in pathologic fibrotic reactions, or, in the setting of microbial invasion, can cooperate with inflammatory cytokines to promote responses by cytotoxic NK cells, Th1 cells and CD8+ T cells. Here, we highlight the regulation and function of IL-33 and ST2, and review their roles in homeostasis, damage and inflammation, suggesting a conceptual framework for future studies.

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“…However, the functional importance of immune cell‐derived IL‐33 in allergic immune responses is not fully understood. Indeed, a recent study showed that IL‐33 produced by tissue cells, but not that produced by immune cells, was essential for allergen‐driven airway inflammation …”

Section: Expression Of Il‐33mentioning

confidence: 99%

IL‐33: biological properties, functions, and roles in airway disease

Drake

Kita

2017

Immunological Reviews

214

203

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Summary Interleukin (IL)-33 is a key cytokine involved in type 2 immunity and allergic airway diseases. Abundantly expressed in lung epithelial cells, IL-33 plays critical roles in both innate and adaptive immune responses in mucosal organs. In innate immunity, IL-33 and group 2 innate lymphoid cells (ILC2s) provide an essential axis for rapid immune responses and tissue homeostasis. In adaptive immunity, IL-33 interacts with dendritic cells, Th2 cells, follicular T cells, and regulatory T cells, where IL-33 influences the development of chronic airway inflammation and tissue remodeling. The clinical findings that both the IL-33 and ILC2 levels are elevated in patients with allergic airway diseases suggest that IL-33 plays an important role in the pathogenesis of these diseases. IL-33 and ILC2 may also serve as biomarkers for disease classification and to monitor the progression of diseases. In this article, we reviewed the current knowledge of the biology of IL-33 and discussed the roles of the IL-33 in regulating airway immune responses and allergic airway diseases.

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IL-33, but Not IL-25, Is Crucial for the Development of House Dust Mite Antigen-Induced Allergic Rhinitis

Cited by 55 publications

References 31 publications

Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa

Dysbiosis-induced IL-33 contributes to impaired antiviral immunity in the genital mucosa

Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation

IL‐33: biological properties, functions, and roles in airway disease

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