H
He Chang
Researcher at Niigata University
Publications - 12
Citations - 372
He Chang is an academic researcher from Niigata University. The author has contributed to research in topics: Gene delivery & T cell. The author has an hindex of 9, co-authored 12 publications receiving 356 citations. Previous affiliations of He Chang include RMIT University.
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Journal ArticleDOI
Hydrodynamic-based delivery of an interleukin-22-Ig fusion gene ameliorates experimental autoimmune myocarditis in rats.
He Chang,Haruo Hanawa,Hui Liu,Tsuyoshi Yoshida,Manabu Hayashi,Ritsuo Watanabe,Satoru Abe,Ken Toba,Kaori Yoshida,Raafat Elnaggar,Shiro Minagawa,Yuji Okura,Kiminori Kato,Makoto Kodama,Hiroki Maruyama,Jun-ichi Miyazaki,Yoshifusa Aizawa +16 more
TL;DR: Results showed that the expression of immunologic molecules in IL-1-stimulated NC cells was significantly decreased by rIL-22 or serum containing IL-22-Ig, and the reason for this effectiveness may be that IL- 22 suppressed gene expression of PG synthases, IL-6, and chemokines in activated NC noninflammatory cells.
Journal ArticleDOI
High expression of IL-22 suppresses antigen-induced immune responses and eosinophilic airway inflammation via an IL-10-associated mechanism
Kazuyuki Nakagome,Mitsuru Imamura,Kimito Kawahata,Hiroaki Harada,Katsuhide Okunishi,Taku Matsumoto,Oh Sasaki,Ryoichi Tanaka,Mitsunobu R. Kano,He Chang,Haruo Hanawa,Jun-ichi Miyazaki,Kazuhiko Yamamoto,Makoto Dohi +13 more
TL;DR: IL-22 could have an immunosuppressive effect during the early stage of an immune response, and IL-10 plays an important role in the immune suppression by IL-22.
Journal ArticleDOI
Alteration of IL-17 related protein expressions in experimental autoimmune myocarditis and inhibition of IL-17 by IL-10-Ig fusion gene transfer.
He Chang,Haruo Hanawa,Tsuyoshi Yoshida,Manabu Hayashi,Hui Liu,Limin Ding,Keita Otaki,Kazuhisa Hao,Kaori Yoshida,Kiminori Kato,Ken Toba,Makoto Kodama,Hiroki Maruyama,Jun-ichi Miyazaki,Yoshifusa Aizawa +14 more
TL;DR: IL-17 is highly produced by αβT cells in the early phase of EAM hearts and IL-17 inhibition might be a possible mechanism of the amelioration of E AM by IL-10-Ig treatment, suggesting that IL- 17 produced by Th17 plays an important role in the pathogenesis of rat EAM.
Journal ArticleDOI
Effect of Hydrodynamics-Based Gene Delivery of Plasmid DNA Encoding Interleukin-1 Receptor Antagonist-Ig for Treatment of Rat Autoimmune Myocarditis Possible Mechanism for Lymphocytes and Noncardiac Cells
Hui Liu,Haruo Hanawa,Tsuyoshi Yoshida,Raafat Elnaggar,Manabu Hayashi,Ritsuo Watanabe,Ken Toba,Kaori Yoshida,He Chang,Yuji Okura,Kiminori Kato,Makoto Kodama,Hiroki Maruyama,Jun-ichi Miyazaki,Mikio Nakazawa,Yoshifusa Aizawa +15 more
TL;DR: EAM was suppressed by hydrodynamics-based delivery of plasmid DNA encoding IL-1RA-Ig and the expression of immune-relevant genes within noncardiomyocytic cells cultured from EAM hearts or concanavalin A-stimulated lymphocytes derived from lymph nodes in EAM-affected rats.
Journal ArticleDOI
Alteration of IL-17 Related Protein Expressions in Experimental Autoimmune Myocarditis and Inhibition of IL-17 by IL-10-Ig Fusion Gene Transfer
Haruo Hanawa,He Chang,Tsuyoshi Yoshida,Manabu Hayashi,Kiminori Kato,Makoto Kodama,Yoshifusa Aizawa +6 more
TL;DR: IL-17 produced by Th17 plays an important role in the pathogenesis of rat EAM, and IL-17 inhibition might be a possible mechanism of the amelioration of EAM by IL-10-Ig treatment.