The role of IL‐33 and its receptor ST2 in human nasal epithelium with allergic rhinitis

  title={The role of IL‐33 and its receptor ST2 in human nasal epithelium with allergic rhinitis},
  author={Ryuta Kamekura and Takashi Kojima and Kenichi Takano and Mitsuru Go and Norimasa Sawada and Tetsuo Himi},
  journal={Clinical \& Experimental Allergy},
Interleukin (IL)‐33 is a novel member of the IL‐1 cytokine family and a ligand for the orphan IL‐1 family receptor ST2. The IL‐33 induces T helper 2‐type inflammatory responses and is considered to play a crucial rule in allergic inflammations, such as asthma and atopic dermatitis. However, the role of IL‐33 and its receptor ST2 in allergic rhinitis remains unknown. 

Expression of IL‐33 and its receptor ST2 in chronic rhinosinusitis with nasal polyps

The role of IL‐33 and its receptor ST2 in chronic rhinosinusitis remains unclear, but it is clear that it plays a crucial role in allergic inflammatory reactions.

Nasal levels of soluble IL‐33R ST2 and IL‐16 in allergic rhinitis: inverse correlation trends with disease severity

Recent studies show that IL‐16, soluble ST2 or anti‐IL‐33 reduce type 2 cytokines (such as IL‐5) and eosinophilia in murine models of allergic asthma or allergic rhinitis respectively.

The Role of Interleukin-33 in Rhinitis

Recent investigations regarding the IL-33/ST2 axis involvement in Th2 inflammatory response and pathogenesis of rhinitis have been reviewed and the role of IL- 33 as a novel promising therapeutic target has also been discussed.

Synergistic relationship between TSLP and IL‐33/ST2 signaling pathways in allergic rhinitis and the effects of hypoxia

The aim of this study was to explore the relationship and expressions and biologic functions of TSLP and IL‐33/ST2 in AR, and also to determine the effects of hypoxia on these cytokines.

Interaction of thymic stromal lymphopoietin, IL‐33, and their receptors in epithelial cells in eosinophilic chronic rhinosinusitis with nasal polyps

Thymic stromal lymphopoietin (TSLP), IL‐25, and IL‐33 system contribute to the initiation and development of Th2 responses in chronic rhinosinusitis with nasal polyps and their cross‐regulation in human nasal epithelial cells (HNECs).

Interleukin-33: Its Emerging Role in Allergic Diseases

The mobilization and biological function of IL-33 in allergic disorders is reviewed, providing novel insights for addressing these hypersensitive conditions.

The IL-33/ST2 axis: Role in health and disease.

Regulation of interleukin‐33 and thymic stromal lymphopoietin in human nasal fibroblasts by proinflammatory cytokines

This work investigated the signal transduction regulation of IL‐33 and TSLP induced by proinflammatory cytokines in nasal fibroblasts and found that these molecules regulated the regulation of epithelial cells and smooth muscle cells at nasal mucosal sites.

Increased expression of IL‐33 is found in the lower airways of patients with seasonal allergic rhinitis and is not related to natural allergen exposure

  • A. HaccuriaA. van Muylem A. Michils
  • Medicine, Biology
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 2021
Evidence of a silent epithelial dysfunction in the airways of patient suffering from allergic rhinitis without asthma is provided, further confirming the «one airway, one disease» theory linking asthma and rhinita.

The role of type 2 innate lymphoid cells in asthma

This work reviews the recent data regarding ILCs and their role in asthma, and newly described cell types that produce a variety of cytokines, including IL‐5 and IL‐13 are reviewed.



Association of serum interleukin‐33 level and the interleukin‐33 genetic variant with Japanese cedar pollinosis

  • M. SakashitaT. Yoshimoto M. Tamari
  • Medicine, Biology
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 2008
Serum levels of IL‐33 and the genetic influences of the polymorphisms ofIL‐33 in human allergic diseases are unclear and type 2 T helper responses are studied.

Disease-associated functions of IL-33: the new kid in the IL-1 family

IL-33 is host-protective against helminth infection and reduces atherosclerosis by promoting TH2-type immune responses but can also promote the pathogenesis of asthma by expanding TH2 cells and mediate joint inflammation, atopic dermatitis and anaphylaxis by mast cell activation.

Characterization of the novel ST2/IL‐33 system in patients with inflammatory bowel disease

The novel association between the ST2/IL‐33 system and IBD seems to identify that variations in this axis might regulate the inflammatory process in these diseases.

IL-33 and IL-33 receptors in host defense and diseases.

The current knowledge regarding the roles of IL-33 andIL-33 receptors in host defense and disease development is summarized and discussed.

Cutting Edge: The ST2 Ligand IL-33 Potently Activates and Drives Maturation of Human Mast Cells1

It is reported that IL-33 directly stimulates primary human mast cells to produce several proinflammatory cytokines and chemokines and also exerts a permissive effect on the MCs response to thymic stromal lymphopoietin, a recently described potent MCs activator.

Human basophils and eosinophils are the direct target leukocytes of the novel IL-1 family member IL-33.

It is demonstrated that basophils and eosinophils are the only direct target leukocytes for IL- 33, suggesting that IL-33 promotes allergic inflammation and Th2 polarization mainly by the selective activation of these specialized cells of the innate immune system.

A novel IL-1 family cytokine, IL-33, potently activates human eosinophils.

An IL-1 Cytokine Member, IL-33, Induces Human Basophil Activation via Its ST2 Receptor1

It is revealed that IL-33 potently regulates migration and activation of human basophils.

Interleukin‐33: a novel mediator with a role in distinct disease pathologies

IL‐33 – a novel mediator with a role in distinct disease pathologies (Key Symposium) and its role in immunity and inflammation is investigated.

IL-33 Amplifies the Polarization of Alternatively Activated Macrophages That Contribute to Airway Inflammation1

It is demonstrated here that IL-33/ST2 plays a significant role in the amplification of AAM polarization and chemokine production which contribute to innate and Ag-induced airway inflammation.