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Perinatal activation of the interleukin-33 pathway promotes type 2 immunity in the developing lung

Ismé De Kleer (UGent) , Mirjam Kool (UGent) , Marjolein JW de Bruijn, Monique Willart (UGent) , Justine Van Moorleghem (UGent) , Martijn Schuijs (UGent) , Maud Plantinga (UGent) , Rudi Beyaert (UGent) , Emily Hams, Padraic G Fallon, et al.
(2016) IMMUNITY. 45(6). p.1285-1298
Author
Organization
Abstract
Allergic disease originates in early life and polymorphisms in interleukin-33 gene (IL33) and IL1RL1, coding for IL-33R and decoy receptor sST2, confer allergy risk. Early life T helper 2 (Th2) cell skewing and allergy susceptibility are often seen as remnants of feto-maternal symbiosis. Here we report that shortly after birth, innate lymphoid type 2 cells (ILC2s), eosinophils, basophils, and mast cells spontaneously accumulated in developing lungs in an IL-33-dependent manner. During the phase of postnatal lung alveolarization, house dust mite exposure further increased IL-33, which boosted cytokine production in ILC2s and activated CD11b(+) dendritic cells (DCs). IL-33 suppressed IL-12p35 and induced OX40L in neonatal DCs, thus promoting Th2 cell skewing. Decoy sST2 had a strong preventive effect on asthma in the neonatal period, less so in adulthood. Thus, enhanced neonatal Th2 cell skewing to inhaled allergens results from postnatal hyperactivity of the IL-33 axis during a period of maximal lung remodeling.
Keywords
HOUSE-DUST MITE, INNATE LYMPHOID-CELLS, DENDRITIC CELLS, T-CELLS, AIRWAY, INFLAMMATION, IMPAIRED RESPONSES, ALVEOLAR FORMATION, NEONATAL IMMUNITY, RESPIRATORY-TRACT, EPITHELIAL-CELLS

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MLA
De Kleer, Ismé, et al. “Perinatal Activation of the Interleukin-33 Pathway Promotes Type 2 Immunity in the Developing Lung.” IMMUNITY, vol. 45, no. 6, 2016, pp. 1285–98, doi:10.1016/j.immuni.2016.10.031.
APA
De Kleer, I., Kool, M., de Bruijn, M. J., Willart, M., Van Moorleghem, J., Schuijs, M., … Lambrecht, B. (2016). Perinatal activation of the interleukin-33 pathway promotes type 2 immunity in the developing lung. IMMUNITY, 45(6), 1285–1298. https://doi.org/10.1016/j.immuni.2016.10.031
Chicago author-date
De Kleer, Ismé, Mirjam Kool, Marjolein JW de Bruijn, Monique Willart, Justine Van Moorleghem, Martijn Schuijs, Maud Plantinga, et al. 2016. “Perinatal Activation of the Interleukin-33 Pathway Promotes Type 2 Immunity in the Developing Lung.” IMMUNITY 45 (6): 1285–98. https://doi.org/10.1016/j.immuni.2016.10.031.
Chicago author-date (all authors)
De Kleer, Ismé, Mirjam Kool, Marjolein JW de Bruijn, Monique Willart, Justine Van Moorleghem, Martijn Schuijs, Maud Plantinga, Rudi Beyaert, Emily Hams, Padraic G Fallon, Hamida Hammad, Rudi W Hendriks, and Bart Lambrecht. 2016. “Perinatal Activation of the Interleukin-33 Pathway Promotes Type 2 Immunity in the Developing Lung.” IMMUNITY 45 (6): 1285–1298. doi:10.1016/j.immuni.2016.10.031.
Vancouver
1.
De Kleer I, Kool M, de Bruijn MJ, Willart M, Van Moorleghem J, Schuijs M, et al. Perinatal activation of the interleukin-33 pathway promotes type 2 immunity in the developing lung. IMMUNITY. 2016;45(6):1285–98.
IEEE
[1]
I. De Kleer et al., “Perinatal activation of the interleukin-33 pathway promotes type 2 immunity in the developing lung,” IMMUNITY, vol. 45, no. 6, pp. 1285–1298, 2016.
@article{8510902,
  abstract     = {{Allergic disease originates in early life and polymorphisms in interleukin-33 gene (IL33) and IL1RL1, coding for IL-33R and decoy receptor sST2, confer allergy risk. Early life T helper 2 (Th2) cell skewing and allergy susceptibility are often seen as remnants of feto-maternal symbiosis. Here we report that shortly after birth, innate lymphoid type 2 cells (ILC2s), eosinophils, basophils, and mast cells spontaneously accumulated in developing lungs in an IL-33-dependent manner. During the phase of postnatal lung alveolarization, house dust mite exposure further increased IL-33, which boosted cytokine production in ILC2s and activated CD11b(+) dendritic cells (DCs). IL-33 suppressed IL-12p35 and induced OX40L in neonatal DCs, thus promoting Th2 cell skewing. Decoy sST2 had a strong preventive effect on asthma in the neonatal period, less so in adulthood. Thus, enhanced neonatal Th2 cell skewing to inhaled allergens results from postnatal hyperactivity of the IL-33 axis during a period of maximal lung remodeling.}},
  author       = {{De Kleer, Ismé and Kool, Mirjam and de Bruijn, Marjolein JW and Willart, Monique and Van Moorleghem, Justine and Schuijs, Martijn and Plantinga, Maud and Beyaert, Rudi and Hams, Emily and Fallon, Padraic G and Hammad, Hamida and Hendriks, Rudi W and Lambrecht, Bart}},
  issn         = {{1074-7613}},
  journal      = {{IMMUNITY}},
  keywords     = {{HOUSE-DUST MITE,INNATE LYMPHOID-CELLS,DENDRITIC CELLS,T-CELLS,AIRWAY,INFLAMMATION,IMPAIRED RESPONSES,ALVEOLAR FORMATION,NEONATAL IMMUNITY,RESPIRATORY-TRACT,EPITHELIAL-CELLS}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{1285--1298}},
  title        = {{Perinatal activation of the interleukin-33 pathway promotes type 2 immunity in the developing lung}},
  url          = {{http://doi.org/10.1016/j.immuni.2016.10.031}},
  volume       = {{45}},
  year         = {{2016}},
}
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