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dc.contributor.authorHadebe, Sabelo
dc.contributor.authorKhumalo, Jermaine
dc.contributor.authorMangali, Sandisiwe
dc.contributor.authorMthembu, Nontobeko
dc.contributor.authorNdlovu, Hlumani
dc.contributor.authorScibiorek, Martyna
dc.contributor.authorNgomti, Amkele
dc.contributor.authorBrombacher, Frank
dc.date.accessioned2021-01-25T07:33:10Z
dc.date.available2021-01-25T07:33:10Z
dc.date.issued2020
dc.identifier.citations: Hadebe S, Khumalo J, Mangali S, Mthembu N, Ndlovu H, Scibiorek M,Ngomti A, Kirstein F, Brombacher F, Deletion of IL-4Rα signalling on B cells limits hyperresponsivenessdepending on antigen-load., Journal of Allergy and Clinical Immunology (2021)en_US
dc.identifier.urihttp://hdl.handle.net/10566/5735
dc.description.abstractB cells play an important role in allergies through secretion of IgE. Interleukin 4 50 receptor α (IL-4Rα) is key in allergic asthma and regulates type 2 cytokine production, IgE 51 secretion and airway hyperresponsiveness (AHR). IL-4 activation of B cells is essential for 52 class-switching and contributes to the induction of B effector 2 (Be2) cells. The role of Be2 53 cells and signalling via IL-4Rα in B cells is not clearly defined.en_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectIL-4Rαen_US
dc.subjectTH2 cellsen_US
dc.subjectB cellsen_US
dc.subjectgerminal centreen_US
dc.subjectT follicular helper cellen_US
dc.subjectB effector 2 cellsen_US
dc.titleDeletion of IL-4Rα signalling on B cells limits hyperresponsiveness depending on antigen-load.en_US
dc.typeArticleen_US


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