Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/53591
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dc.contributor.authorAsquith, K.-
dc.contributor.authorRamshaw, H.-
dc.contributor.authorHansbro, P.-
dc.contributor.authorBeagley, K.-
dc.contributor.authorLopez, A.-
dc.contributor.authorFoster, P.-
dc.date.issued2008-
dc.identifier.citationJournal of Immunology, 2008; 180(2):1199-1206-
dc.identifier.issn0022-1767-
dc.identifier.issn1550-6606-
dc.identifier.urihttp://hdl.handle.net/2440/53591-
dc.descriptionCopyright © 2008 by The American Association of Immunologists, Inc.-
dc.description.abstractThe eosinophil is a central effector cell in allergic asthma. Differentiation and function of eosinophils are regulated by the CD4 Th2 cytokines IL-3, IL-5, and GM-CSF, which all signal through a common beta receptor subunit (betac). Recent therapeutic approaches targeting IL-5 alone have not ablated tissue accumulation of eosinophils and have had limited effects on disease progression, suggesting important roles for IL-3 and GM-CSF. By using a mouse model of allergic airways inflammation, we show that allergen-induced expansion and accumulation of eosinophils in the lung are abolished in betac-deficient (betac-/-) mice. Moreover, betac deficiency resulted in inhibition of hallmark features of asthma, including airways hypersensitivity, mucus hypersecretion, and production of Ag-specific IgE. Surprisingly, we also identified a critical role for this receptor in regulating type 2 immunity. Th2 cells in the lung of allergen-challenged betac-/- mice were limited in their ability to proliferate, produce cytokines, and migrate to effector sites, which was attributed to reduced numbers of myeloid dendritic cells in the lung compartment. Thus, the betac plays a critical role in allergen-induced eosinophil expansion and infiltration and is pivotal in regulating molecules that promote both early and late phases of allergic inflammation, representing a novel target for therapy.-
dc.description.statementofresponsibilityKelly L. Asquith, Hayley S. Ramshaw, Philip M. Hansbro, Kenneth W. Beagley, Angel F. Lopez and Paul S. Foster-
dc.language.isoen-
dc.publisherAmer Assoc Immunologists-
dc.source.urihttp://www.jimmunol.org/cgi/content/abstract/180/2/1199-
dc.subjectDendritic Cells-
dc.subjectEosinophils-
dc.subjectTh2 Cells-
dc.subjectMacrophages, Alveolar-
dc.subjectAnimals-
dc.subjectMice-
dc.subjectMice, Mutant Strains-
dc.subjectAsthma-
dc.subjectRespiratory Hypersensitivity-
dc.subjectGranulocyte-Macrophage Colony-Stimulating Factor-
dc.subjectInterleukin-3-
dc.subjectInterleukin-5-
dc.subjectAllergens-
dc.subjectCytokines-
dc.subjectLymphocyte Activation-
dc.subjectSignal Transduction-
dc.subjectCell Movement-
dc.subjectCytokine Receptor Common beta Subunit-
dc.titleThe IL-3/IL-5/GM-CSF common beta receptor plays a pivotal role in the regulation of Th2 immunity and allergic airway inflammation-
dc.typeJournal article-
dc.identifier.doi10.4049/jimmunol.180.2.1199-
pubs.publication-statusPublished-
dc.identifier.orcidRamshaw, H. [0000-0001-9909-282X]-
dc.identifier.orcidLopez, A. [0000-0001-7430-0135]-
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