H
Hajime Takeuchi
Researcher at Tokushima Bunri University
Publications - 12
Citations - 1831
Hajime Takeuchi is an academic researcher from Tokushima Bunri University. The author has contributed to research in topics: Retinoic acid & Retinoid X receptor. The author has an hindex of 9, co-authored 11 publications receiving 1716 citations.
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Journal ArticleDOI
Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells
J. Rodrigo Mora,Makoto Iwata,Bertus Eksteen,Si-Young Song,Tobias Junt,Balimkiz Senman,Kevin L. Otipoby,Aya Yokota,Hajime Takeuchi,Paola Ricciardi-Castagnoli,Klaus Rajewsky,David H. Adams,Ulrich H. von Andrian +12 more
TL;DR: It is shown that dendritic cells from GALT induce T cell–independent expression of IgA and gut-homing receptors on B cells, which shape mucosal immunity by modulating B cell migration and effector activity through synergistically acting mediators.
Journal ArticleDOI
Regulation of IgA production by naturally occurring TNF/iNOS-producing dendritic cells
Hiroyuki Tezuka,Yukiko Abe,Makoto Iwata,Hajime Takeuchi,Hiromichi Ishikawa,Masayuki Matsushita,Tetsuo Shiohara,Shizuo Akira,Toshiaki Ohteki +8 more
TL;DR: It is shown that IgA class-switch recombination (CSR) is impaired in inducible-nitric-oxide-synthase-deficient (iNOS-/-; gene also called Nos2) mice, and the presence of a naturally occurring TNF-α/iNos-producing dendritic-cell subset may explain the predominance of IgA production in the MALT, critical for gut homeostasis.
Journal ArticleDOI
GM-CSF and IL-4 synergistically trigger dendritic cells to acquire retinoic acid-producing capacity
Aya Yokota,Hajime Takeuchi,Naoko Maeda,Yoshiharu Ohoka,Chieko Kato,Si-Young Song,Makoto Iwata +6 more
TL;DR: The results suggest that GM-CSF and RA itself are pivotal among multiple microenvironment factors that enable intestinal DCs to produce RA.
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Cyp26b1 regulates retinoic acid-dependent signals in T cells and its expression is inhibited by transforming growth factor-β.
TL;DR: A role for CYP26b11 in regulating RA-dependent signals in activated T cells but not during TGF-β-dependent differentiation to Foxp3+ regulatory T cells is demonstrated.
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Retinoic Acid-Induced CCR9 Expression Requires Transient TCR Stimulation and Cooperativity between NFATc2 and the Retinoic Acid Receptor/Retinoid X Receptor Complex
TL;DR: The results suggest that the cooperativity between NFATc2 and the RAR/RXR complex is essential for CCR9 expression on T cells and thatNFATc1 interferes with the action of NFAT c2.