2013
DOI: 10.1038/ncomms3675
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Thymic stromal lymphopoietin induces corticosteroid resistance in natural helper cells during airway inflammation

Abstract: Type-2 innate immune responses that occur in airways and are accompanied by goblet-cell hyperplasia and mucus production are largely driven by interleukin-33 (IL-33) and natural helper (NH) cells, a member of group 2 innate lymphoid cells (ILC2s) and the major target of IL-33. Here we report that the corticosteroid resistance observed as a result of airway inflammation triggered by sensitization and exposure to allergen is induced via the IL-33/NHcell axis. Thymic stromal lymphopoietin (TSLP) synthesized durin… Show more

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Cited by 279 publications
(250 citation statements)
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References 42 publications
(50 reference statements)
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“…ILC2 numbers are increased in sputum and peripheral blood of patients with severe asthma compared to mild asthmatics or healthy controls [45,46]. Importantly, evidence was found for a role of uncontrolled localized production of IL-5 and IL-13 by a steroid-insensitive population of ILC2s, in agreement with in vitro studies showing that ILC2s are steroidinsensitive in the presence of TSLP [46,47].In conclusion, the contribution of ILC2s to asthma is related to the properties of the allergen. In papain-induced inflammation, ILC2s are rapidly induced prior to T-cell activation and ILC2-derived IL-13 is essential for the initiation of T-cell activation and Th2 differentiation [13].…”
supporting
confidence: 73%
“…ILC2 numbers are increased in sputum and peripheral blood of patients with severe asthma compared to mild asthmatics or healthy controls [45,46]. Importantly, evidence was found for a role of uncontrolled localized production of IL-5 and IL-13 by a steroid-insensitive population of ILC2s, in agreement with in vitro studies showing that ILC2s are steroidinsensitive in the presence of TSLP [46,47].In conclusion, the contribution of ILC2s to asthma is related to the properties of the allergen. In papain-induced inflammation, ILC2s are rapidly induced prior to T-cell activation and ILC2-derived IL-13 is essential for the initiation of T-cell activation and Th2 differentiation [13].…”
supporting
confidence: 73%
“…Levels of IL-33 correlated with increased reticular basement membrane thickness in endobronchial biopsies, and mouse studies in which neonatal mice were dosed with house dust mite allergens indicated that, in contrast to IL-13 levels, IL-33 concentrations were steroid resistant. A similar link between IL-33 stimulation in the context of ovalbumin (OVA) challenge in the lung and steroid resistance was recently reported to be due to TSLP (61). When mice were dosed with only IL-33, the inflammatory response could be inhibited by treatment with dexamethasone.…”
Section: Ilc2 In Lung Allergy and Inflammationmentioning
confidence: 79%
“…Subsequently, the predominantly epithelial cell-derived cytokine thymic stromal lymphopoietin (TSLP) has also been shown to be a key regulator of ILC2 function (Halim et al 2012a;Kim et al 2013a). Recent studies have shown that TSLP induces GATA3 expression in human ILC2s (Mjosberg et al 2012) and promotes corticosteroid resistance to IL-33-mediated activation of ILC2s in the lung (Kabata et al 2013). In addition, enforced expression of GATA3 in T cells and ILC2s results in elevated expression of IL-5 and IL-13 and enhanced susceptibility to allergic airway disease in mice (Kleinjan et al 2014).…”
Section: Regulation and Effector Functions Of Ilc2smentioning
confidence: 99%
“…A recent study has shown that TSLP can contribute to ILC2 activation that promotes corticosteroid resistance in the context of IL-33-mediated airway inflammation (Kabata et al 2013). Further, recent reports suggest that other factors, such as eicosanoids, could also play a key role in promoting ILC2 responses in the inflamed lung (Barnig et al 2013;Doherty et al 2013).…”
Section: Ilc2s and Allergic Airway Inflammationmentioning
confidence: 99%