H
Hideaki Morita
Researcher at Swiss Institute of Allergy and Asthma Research
Publications - 121
Citations - 5454
Hideaki Morita is an academic researcher from Swiss Institute of Allergy and Asthma Research. The author has contributed to research in topics: Innate lymphoid cell & Interleukin 33. The author has an hindex of 29, co-authored 102 publications receiving 4197 citations. Previous affiliations of Hideaki Morita include Keio University & University of Zurich.
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Journal ArticleDOI
IL-33 is a crucial amplifier of innate rather than acquired immunity
Keisuke Oboki,Tatsukuni Ohno,Naoki Kajiwara,Ken Arae,Hideaki Morita,Akina Ishii,Aya Nambu,Takaya Abe,Hiroshi Kiyonari,Kenji Matsumoto,Katsuko Sudo,Ko Okumura,Hirohisa Saito,Susumu Nakae +13 more
TL;DR: It is found that IL-1, but not IL-33, played a substantial role in induction of T cell-mediated type IV hypersensitivity such as contact and delayed-type hypersensitivity and autoimmune diseases such as experimental autoimmune encephalomyelitis andIL-33 was important for innate-type mucosal immunity in the lungs and gut.
Journal ArticleDOI
Interleukins (from IL-1 to IL-38), interferons, transforming growth factor β, and TNF-α: Receptors, functions, and roles in diseases
Mübeccel Akdis,Alar Aab,Can Altunbulakli,Kursat A Azkur,Rita Costa,Reto Crameri,Su Duan,Thomas Eiwegger,Andrzej Eljaszewicz,Ruth Ferstl,Remo Frei,Mattia Garbani,Anna Głobińska,Lena Hess,Carly Huitema,Terufumi Kubo,Zsolt István Komlósi,Patricia Konieczna,Nóra Kovács,Umut Can Kucuksezer,Norbert Meyer,Hideaki Morita,Judith Olzhausen,Liam O'Mahony,Marija Pezer,Moira Prati,Ana Rebane,Claudio Rhyner,Arturo Rinaldi,Milena Sokolowska,Barbara Stanic,Kazunari Sugita,Angela Treis,Willem van de Veen,Kerstin Wanke,Marcin Wawrzyniak,Paulina Wawrzyniak,Oliver F. Wirz,Josefina Zakzuk,Cezmi A. Akdis +39 more
TL;DR: Recent developments on IL-1 to IL-38, TNF-α, TGF-β, and interferons are reviewed and their cellular sources, targets, receptors, signaling pathways, and roles in immune regulation in patients with allergy and asthma and other inflammatory diseases are discussed.
Journal ArticleDOI
Application of moisturizer to neonates prevents development of atopic dermatitis
Kenta Horimukai,Kumiko Morita,Masami Narita,Mai Kondo,Hiroshi Kitazawa,Makoto Nozaki,Yukiko Shigematsu,Kazue Yoshida,Hironori Niizeki,Kenichiro Motomura,Haruhiko Sago,Tetsuya Takimoto,Eisuke Inoue,Norio Kamemura,Hiroshi Kido,Junzo Hisatsune,Motoyuki Sugai,Hiroyuki Murota,Ichiro Katayama,Takashi Sasaki,Masayuki Amagai,Hideaki Morita,Akio Matsuda,Kenji Matsumoto,Hirohisa Saito,Yukihiro Ohya +25 more
TL;DR: Daily application of moisturizer during the first 32 weeks of life reduces the risk of AD/eczema in infants and allergic sensitization during this time period is associated with the presence of eczematous skin but not with moisturizer use.
Journal ArticleDOI
Distribution of ACE2, CD147, CD26, and other SARS-CoV-2 associated molecules in tissues and immune cells in health and in asthma, COPD, obesity, hypertension, and COVID-19 risk factors.
Urszula Radzikowska,Urszula Radzikowska,Mei Ding,Mei Ding,Ge Tan,Ge Tan,Damir Zhakparov,Yaqi Peng,Paulina Wawrzyniak,Ming Wang,Shuo Li,Hideaki Morita,Can Altunbulakli,Matthias Reiger,Avidan U. Neumann,Avidan U. Neumann,Nonhlanhla Lunjani,Claudia Traidl-Hoffmann,Kari C. Nadeau,Liam O'Mahony,Liam O'Mahony,Cezmi A. Akdis,Milena Sokolowska +22 more
TL;DR: The aim of this study was to analyze the expression of known and potential SARS‐CoV‐2 receptors and related molecules in the extensive collection of primary human cells and tissues from healthy subjects of different age and from patients with risk factors and known comorbidities of COVID‐19.
Journal ArticleDOI
Basophil-derived interleukin-4 controls the function of natural helper cells, a member of ILC2s, in lung inflammation
Yasutaka Motomura,Hideaki Morita,Kazuyo Moro,Kazuyo Moro,Susumu Nakae,David Artis,Takaho A. Endo,Yoko Kuroki,Osamu Ohara,Shigeo Koyasu,Masato Kubo +10 more
TL;DR: It is found that basophils play a crucial role in NH cell-mediated eosinophilic inflammation induced by protease allergens, subsequently leading to protease allergen-induced airway inflammation.