IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC–activated Th2 memory cells
By Yui-Hsi Wang, P. Angkasekwinai, Ning Lu, K. Voo, K. Arima, S. Hanabuchi, A. Hippe, C. Corrigan, C. Dong, B. Homey and 4 more. Journal of Experimental Medicine, 2007
685 citations recorded by the source corpus.
Interleukin (IL) 25 (IL-17E), a distinct member of the IL-17 cytokine family, plays important roles in evoking T helper type 2 (Th2) cell–mediated inflammation that features the infiltrations of eosinophils and Th2 memory cells. However, the cellular sources, target cells, and underlying mechanisms remain elusive in humans. We demonstrate that human Th2 memory cells expressing distinctive levels of IL-25 receptor (R) are one of the responding cell types. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin (TSLP)–activated dendritic cells (DCs), homeostatic cytokines, or T cell receptor for antigen triggering. The enhanced functions of Th2 memory cells induced by IL-25 are associated with sustained expression of GATA-3, c-MAF, and JunB in an IL-4–independent manner. Although keratinocytes, mast cells, eosinophils, and basophils express IL-25 transcripts, activated eosinophils and basophils from normal and atopic subjects were found to secrete bioactive IL-25 protein, which augments the functions of Th2 memory cells. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. Our results provide a plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells.
Subfields: Dermatology, Physiology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/3f281e9cb35e31d059b395235483d53e0fdc0cbd
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Citations in the corpus
- A role for IL-25 and IL-33–driven type-2 innate lymphoid cells in atopic dermatitis (2013, result): “This would be consistent with the fact that an increase in IL-33 mRNA is reported in the lesional skin biopsies of patients with AD compared with healthy individuals (Miller, 2011), and IL-25 is also found in higher concentrations in these patients (Wang et al., 2007; Hvid et al., 2011).”
- A critical function for transforming growth factor-β, interleukin 23 and proinflammatory cytokines in driving and modulating human TH-17 responses (2008, background): “However, we did not detect measurable amounts of other IL-17 family members, such as IL-17E (IL-25), which is related more to T H 2 response”
- How are TH2-type immune responses initiated and amplified? (2010, background): “Increased IL-25 and IL-25R expression have been detected in patients with asthma suggesting that IL-25 may serve as an amplification factor in human allergic disease”
- The cytokine network in asthma and chronic obstructive pulmonary disease. (2008, background): “It also enhances Th2 cytokine secretion from human Th2 cells (48).”
- Th2 Cytokines and Atopic Dermatitis (2011, background): “Two studies have demonstrated that mRNA and protein levels of IL-25 and it cognate receptor, IL-25R are elevated in the skin of individuals with AD, and their expression is higher in lesional skin compared to non-lesional skin [44,45].”