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Title: Basophils are required for the induction of Th2 immunity to haptens and peptide antigens
Authors: Otsuka, Atsushi  KAKEN_id
Nakajima, Saeko  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0003-0831-1447 (unconfirmed)
Kubo, Masato
Egawa, Gyohei  KAKEN_id
Honda, Tetsuya  KAKEN_id
Kitoh, Akihiko  KAKEN_id
Nomura, Takashi
Hanakawa, Sho
Sagita Moniaga, Catharina
Kim, Bongju
Matsuoka, Satoshi
Watanabe, Takeshi
Miyachi, Yoshiki
Kabashima, Kenji  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0002-0773-0554 (unconfirmed)
Author's alias: 大塚, 篤司
宮地, 良樹
椛島, 健治
Keywords: Biological sciences
Immunology
Issue Date: 23-Apr-2013
Publisher: Nature Publishing Group
Journal title: Nature Communications
Volume: 4
Thesis number: 1738
Abstract: The relative contributions of basophils and dendritic cells in Th2 skewing to foreign antigen exposure remain unclear. Here we report the ability of basophils to induce Th2 polarization upon epicutaneous sensitization with different antigens using basophil conditionally depleted Bas TRECK transgenic mice. Basophils are responsible for Th2 skewing to haptens and peptide antigens, but not protein antigens in vivo. Consistent with this, basophils cannot take up or process ovalbumin protein in significant quantities, but present ovalbumin peptide to T cells for Th2 differentiation via major histocompatibility complex class II. Intriguingly, basophils promote Th2 skewing upon ovalbumin protein exposure in the presence of dendritic cells. Taken together, our results suggest that basophils alone are able to induce Th2 skewing with haptens and peptide antigens but require dendritic cells for the induction of Th2 for protein antigens upon epicutaneous immunization.
Description: ハプテンやペプチド抗原に対するTh2誘導に好塩基球が必須である. 京都大学プレスリリース. 2013-04-24.
Rights: © 2013 Nature Publishing Group
This work is licensed under a Creative Commons Attribution-NonCommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/
URI: http://hdl.handle.net/2433/173564
DOI(Published Version): 10.1038/ncomms2740
PubMed ID: 23612279
Related Link: https://www.kyoto-u.ac.jp/static/ja/news_data/h/h1/news6/2013/130424_2.htm
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