Interleukin-25 and mucosal T cells in noneosinophilic and eosinophilic chronic rhinosinusitis

Iinuma, Tomohisa; Okamoto, Yoshitaka; Yamamoto, Heizaburo; Inamine-Sasaki, Ayako; Ohki, Yuji; Sakurai, Takeshi; Funakoshi, Urara; Yonekura, Syuji; Sakurai, Daiju; Hirahara, Kiyoshi; Nakayama, Toshinori

doi:10.1016/j.anai.2015.01.013

Cited by 49 publications

(45 citation statements)

References 46 publications

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“…IL-25 has been shown to stimulate their proliferation as well as enhance Th2 polarization and cytokine production by up-regulating the expression of transcription factors like GATA-3 and c-MAF (34, 35). Increased IL17RB transcripts were also reported in CD4 + T cells isolated from nasal polyps of patients with eosinophilic chronic rhinosinusitis (36) and in circulating CD4 + T cells following nasal allergen challenge (37). Several studies in animal models have consistently shown that IL-25, like the other prototypical type 2 cytokines IL-5, IL-13 and IL-4, promote pathogenic Th2 cell-mediated inflammatory responses in the lung (34, 38).…”

Section: Resultsmentioning

confidence: 90%

Transcriptional Profiling of Th2 Cells Identifies Pathogenic Features Associated with Asthma

Seumois

Zapardiel‐Gonzalo

White

et al. 2016

The Journal of Immunology

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Allergic asthma and rhinitis are two common chronic allergic diseases that affect the lungs and nose, respectively. Both diseases share clinical and pathological features characteristic of excessive allergen-induced type 2 inflammation, orchestrated by memory CD4+ T cells that produce type 2 cytokines (Th2 cells). However, a large majority of subjects with allergic rhinitis do not develop asthma, suggesting divergence in disease mechanisms. Since Th2 cells play a pathogenic role in both these diseases and are also present in healthy non-allergic subjects, we performed global transcriptional profiling to determine whether there are qualitative differences in Th2 cells from subjects with allergic asthma, rhinitis and healthy controls. Th2 cells from asthmatic subjects expressed higher levels of several genes that promote their survival as well as alter their metabolic pathways to favor persistence at sites of allergic inflammation. In addition, genes that enhanced Th2 polarization and Th2 cytokine production were also upregulated in asthma. Several genes that oppose T cell activation were downregulated in asthma, suggesting enhanced activation potential of Th2 cells from asthmatic subjects. Many novel genes with poorly defined functions were also differentially expressed in asthma. Thus, our transcriptomic analysis of circulating Th2 cells has identified several molecules that are likely to confer pathogenic features to Th2 cells that are either unique or common to both asthma and rhinitis.

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Section: Resultsmentioning

confidence: 90%

Transcriptional Profiling of Th2 Cells Identifies Pathogenic Features Associated with Asthma

Seumois

Zapardiel‐Gonzalo

White

et al. 2016

The Journal of Immunology

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“…It has been shown that the respiratory epithelium mediates the Th2 response through producing a series of epitheliumderived cytokines, including IL-25, IL-33, and thymic stromal lymphopoietin [70]. Interestingly, IL-25, IL-33, and thymic stromal lymphopoietin were significantly increased in eosinophilic CRSwNP cases compared with noneosinophilic counterparts, and they were recently found to play an essential role in regulating both the innate immunity and adaptive immunity in sinus mucosa [71][72][73]. They are able to activate both pro-Th2-skewed dendritic cells and group 2 innate lymphoid cells.…”

Section: The Implications Of Short Palate Lung and Nasal Epithelialmentioning

confidence: 95%

Differential short palate, lung, and nasal epithelial clone 1 suppression in eosinophilic and noneosinophilic chronic rhinosinusitis with nasal polyps

Wei

Han

Wen

et al. 2016

Current Opinion in Allergy &Amp; Clinical Immunology

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“…Additionally, polyp-derived IL-17RB (+) Th2 cells were identified in NP, which co-expressed ST2 and enhanced IL-5 and IL-13 production in response to IL-25 and IL-33 34. Protein levels of IL-25 are up-regulated in non-eosinophilic NP as well as eosinophilic NP 2235. Of note, the fact that IL-25, known as a cytokine involved in diverse Th2-mediated diseases, also correlated with inflammatory mediators involved in Th1 and Th17 responses in Asian subjects suggests that it may play diverse roles in polypogenesis besides promoting Th2 inflammation 3336.…”

Section: Pathogenesis and Endotypes Of Crsmentioning

confidence: 98%

Emerging Endotypes of Chronic Rhinosinusitis and Its Application to Precision Medicine

Kim

Cho

2017

Allergy Asthma Immunol Res

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Chronic rhinosinusitis (CRS) is a heterogeneous inflammatory disease with various underlying pathophysiologic mechanisms which translate to endotypes, in contrast to clinical phenotypes or histological subtypes. Defining endotypes can help clinicians predict disease prognosis, select subjects suitable for a specific therapy, and assess risks for comorbid conditions, including asthma. Therefore, with recent advancement of biologicals in CRS clinical trials, endotyping can be a breakthrough in treating recalcitrant CRS. CRS is caused by dysregulated immunologic responses to external stimuli, which induce various inflammatory mediators from inflammatory cells, including innate lymphoid cells (ILCs) and T lymphocytes as well as epithelial cells. Thymic stromal lymphopoietin (TSLP), interleukin (IL)-25, and IL-33, which are mainly secreted by epithelial cells in response to external stimuli, act on type 2 ILCs and T helper 2 (Th2) cells, inducing IL-4, IL-5, and IL-13. Local immunoglobulin E (IgE) production is also a signature event in nasal polyps (NP). These inflammatory mediators are novel potential therapeutic targets for recalcitrant CRS. This article reviews recent publications regarding endotypes and endotype-based therapeutic strategies in CRS and NP.

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Interleukin-25 and mucosal T cells in noneosinophilic and eosinophilic chronic rhinosinusitis

Abstract: Interleukin-25 and a subpopulation of tissue T-helper type 2 and 9 cells that express increased IL-17RB levels could contribute to infiltration of eosinophils in NPs and could have produced the pathologic difference between NECRS and ECRS.

Cited by 49 publications

References 46 publications

Transcriptional Profiling of Th2 Cells Identifies Pathogenic Features Associated with Asthma

Transcriptional Profiling of Th2 Cells Identifies Pathogenic Features Associated with Asthma

Differential short palate, lung, and nasal epithelial clone 1 suppression in eosinophilic and noneosinophilic chronic rhinosinusitis with nasal polyps

Emerging Endotypes of Chronic Rhinosinusitis and Its Application to Precision Medicine

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