Tissue-Restricted Adaptive Type 2 Immunity Is Orchestrated by Expression of the Costimulatory Molecule OX40L on Group 2 Innate Lymphoid Cells
Timotheus Y.F. Halim(MRC Laboratory of Molecular Biology), Batika M.J. Rana(MRC Laboratory of Molecular Biology), Jennifer A. Walker(MRC Laboratory of Molecular Biology), Bernhard Kerscher(MRC Laboratory of Molecular Biology), Martin Knolle(MRC Laboratory of Molecular Biology), Helen E. Jolin(MRC Laboratory of Molecular Biology), Eva Serrão(University of Cambridge), Liora Haim-Vilmovsky(Wellcome Sanger Institute), Sarah A. Teichmann(Wellcome Sanger Institute), Hans‐Reimer Rodewald(German Cancer Research Center), Marina Botto(Imperial College London), Timothy J. Vyse(King's College London), Padraic G. Fallon(Trinity College Dublin), Zhi Li(University of Birmingham), David R. Withers(University of Birmingham), Andrew N. J. McKenzie(MRC Laboratory of Molecular Biology)
Cited by 239Open Access
Abstract
mice failed to mount effective Th2 and Treg cell responses and corresponding adaptive type 2 pulmonary inflammation arising from Nippostrongylus brasiliensis infection or allergen exposure. Thus, the increased expression of OX40L in response to IL-33 acts as a licensing signal in the orchestration of tissue-specific adaptive type 2 immunity, without which this response fails to establish.
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