The Role of Regulatory T Cells in the Regulation of Upper Airway Inflammation

Palmer, Charlie; Mulligan, Jennifer K.; Smith, Sarah E.; Atkinson, Carl

doi:10.2500/ajra.2017.31.4472

Cited by 28 publications

(18 citation statements)

References 88 publications

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“…Moreover, Foxp3 levels in an organism can directly reflect the quantity and functional status of Treg cells [28]. A decrease in the number of Treg cells or the loss of function and abnormalities of the key transcription factor Foxp3 are closely related to the pathogenesis of AR [29]. It was demonstrated that inhibition of Notch signaling specifically promotes Foxp3 expression and upregulates the differentiation of Treg cells, thereby reducing the inflammatory response associated with AR.…”

Section: Discussionmentioning

confidence: 99%

Notch Signaling Promotes Development of Allergic Rhinitis by Suppressing Foxp3 Expression and Treg Cell Differentiation

Jiao

Wei

Kong

et al. 2018

Int Arch Allergy Immunol

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Background: The Notch signaling pathway plays an important role in regulating human immune function, but the relationship between allergic rhinitis (AR) and Notch signaling remains unclear. Objective: To investigate the role of Notch signaling in the pathogenesis of AR and its regulation on Foxp3-Treg cells. Method: The sera of 100 patients with AR and 50 controls were collected to assess the differences in Notch1, Jagged1, and DLL1 (Delta-like 1) expression. Experimental mice were divided into normal control, AR, Notch inhibitor, and dexamethasone groups. Allergic symptoms, total IgE levels, and the proportion of Treg cells in the peripheral blood were detected. Notch1, Jagged1, NICD (Notch intracellular domain, also known as ICN), and Foxp3 expression and Th1/Th2/Th17-related cytokines in the spleen were detected and compared between each group of mice. Results: Compared with the control group, the expression of Notch1 and Jagged1 in patients with AR was significantly elevated (p < 0.05). The expression of Notch1 and Jagged1 in patients with severe AR was higher than that observed in the mild to moderate AR patients and positively correlated with the levels of allergen sIgE (p < 0.05). The animal experiments revealed that compared with the normal control group, the expression of Notch1, Jagged1, and NICD in the AR group was increased, Foxp3 expression was decreased, and the proportion of Treg cells was decreased (p < 0.05). Compared with the AR group, allergic symptoms and total serum IgE levels and the expression of Notch1, Jagged1, and NICD were significantly decreased in the Notch inhibited group, whereas the expression of Foxp3 and the proportion of Treg cells were increased significantly (p < 0.05). The Th2-type immune responses were also enhanced and Th1-type immune responses decreased in the AR group, but the Th1/Th2 imbalance was reversed in the Notch inhibited group. Conclusion: Notch signaling downregulates Foxp3 expression and inhibits the differentiation of Treg cells to promote the development of AR. Blocking Notch signaling may be a potential treatment for AR.

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Section: Discussionmentioning

confidence: 99%

Notch Signaling Promotes Development of Allergic Rhinitis by Suppressing Foxp3 Expression and Treg Cell Differentiation

Jiao

Wei

Kong

et al. 2018

Int Arch Allergy Immunol

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“…In mice sensitized to ovalbumin, Treg cells inhibited allergen-specific IgE responses and affected allergen-specific Th2 cell priming both in terms of proliferative responses and cytokine secretion 10 . In contrast, the depletion of Treg cells during the sensitization phase of allergy development resulted in a dramatic exacerbation of allergic inflammation 11 . In patients with AR, circulating Treg cell numbers in the peripheral blood of patients were either lower than, or equivalent to, those in control patients 12, 13, 14.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 signal inhibits T regulatory cell differentiation during allergic rhinitis inflammation through EP4 receptor

Li¹,

Guan²,

Zhou

et al. 2019

World Allergy Organization Journal

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ObjectiveAllergic rhinitis (AR) is a common disease seriously affecting quality of life, and until now the effect of medical therapy is not satisfactory. It is essential to explore in depth the pathologic mechanism of AR to offer new ideas for developing novel treatment strategies. The defect of T regulatory (Treg) cells plays a critical role in the pathogenesis of AR, but the underlying mechanism remains to be elucidated. This study aims to determine the effect of Prostaglandin E2 (PGE2) on the differentiation of Treg cells in AR patients and the involvement of E prostanoid (EP) receptor signaling pathway.MethodsThe proportion of Treg cells and the level of PGE2 in the peripheral blood of AR patients and healthy controls were compared. Differentiation rate of Treg cells under the influence of various concentrations of PGE2 with or without diverse EP receptor agonists and antagonists were investigated through cell culture and flow cytometry in vitro. The cyclic AMP (cAMP) mimic or protein kinase B (Akt) inhibitor was also added to the culture to evaluate the downstream pathway of EP receptor signaling.ResultsThe proportion of Treg cells decreased and PGE2 concentration increased in the peripheral blood of AR patients compared to healthy controls. PGE2 dose-dependently suppressed the differentiation of Treg cells from both human and mice naïve CD4+ T cells in vitro. This inhibitory effect was mediated through EP4 via a mechanism involving activation of cAMP-dependent proteinkinase A (PKA) signaling pathway.ConclusionPGE2-EP4-cAMP signaling might mediate the development of AR by inhibiting the differentiation of Treg cells.

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“…Se ha planteado también que la disminución de las células T reguladoras se relacionaría con la imposibilidad de suprimir el estado inflamatorio, sin embargo, los resultados de los estudios son controversiales, no existiendo actualmente una explicación satisfactoria de las diferencias en los hallazgos 46 .…”

Section: B) Rol Del Sistema Inmune Adaptativounclassified

Rinosinusitis crónica: Una revisión de su etiopatogenia

et al. 2018

Rev. Otorrinolaringol. Cir. Cabeza Cuello

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The Role of Regulatory T Cells in the Regulation of Upper Airway Inflammation

Abstract: Allergic rhinitis (AR) and chronic rhinosinusitis with nasal polyps (CRSwNP)

Cited by 28 publications

References 88 publications

Notch Signaling Promotes Development of Allergic Rhinitis by Suppressing Foxp3 Expression and Treg Cell Differentiation

Notch Signaling Promotes Development of Allergic Rhinitis by Suppressing Foxp3 Expression and Treg Cell Differentiation

Prostaglandin E2 signal inhibits T regulatory cell differentiation during allergic rhinitis inflammation through EP4 receptor

Rinosinusitis crónica: Una revisión de su etiopatogenia

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