JaLCDOI | 10.18926/AMO/66912 |
---|---|
フルテキストURL | 78_2_095.pdf |
著者 | Itano, Junko| Kiura, Katsuyuki| Maeda, Yoshinobu| Miyahara, Nobuaki| |
抄録 | The lungs are very complex organs, and the respiratory system performs the dual roles of repairing tissue while protecting against infection from various environmental stimuli. Persistent external irritation disrupts the immune responses of tissues and cells in the respiratory system, ultimately leading to respiratory disease. Neuropeptide Y (NPY) is a 36-amino-acid polypeptide and a neurotransmitter that regulates homeostasis. The NPY receptor is a seven-transmembrane-domain G-protein-coupled receptor with six subtypes (Y1, Y2, Y3, Y4, Y5, and Y6). Of these receptors, Y1, Y2, Y4, and Y5 are functional in humans, and Y1 plays important roles in the immune responses of many organs, including the respiratory system. NPY and the Y1 receptor have critical roles in the pathogenesis of asthma, chronic obstructive pulmonary disease, and idiopathic pulmonary fibrosis. The effects of NPY on the airway immune response and pathogenesis differ among respiratory diseases. This review focuses on the involvement of NPY in the airway immune response and pathogenesis of various respiratory diseases. |
キーワード | neuropeptide y Y1 receptor airway immune response bronchial epithelial cells respiratory disease |
Amo Type | Review |
出版物タイトル | Acta Medica Okayama |
発行日 | 2024-04 |
巻 | 78巻 |
号 | 2号 |
出版者 | Okayama University Medical School |
開始ページ | 95 |
終了ページ | 106 |
ISSN | 0386-300X |
NCID | AA00508441 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
著作権者 | Copyright Ⓒ 2024 by Okayama University Medical School |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 38688827 |
JaLCDOI | 10.18926/AMO/66915 |
---|---|
フルテキストURL | 78_2_123.pdf |
著者 | Saeki, Kyosuke| Fujiwara, Hideaki| Seike, Keisuke| Kuroi, Taiga| Nishimori, Hisakazu| Tanaka, Takehiro| Matsuoka, Ken-ichi| Fujii, Nobuharu| Maeda, Yoshinobu| |
抄録 | Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity following allogeneic hematopoietic cell transplantation (HCT), but its pathogenesis remains unclear. Recently, haplo-identical HCT with post-transplant cyclophosphamide (Haplo-HCT with PTCY) was found to achieve a low incidence rate of acute GVHD and chronic GVHD. However, while the pathogenesis of acute GVHD following Haplo-HCT with PTCY has been well investigated, that of chronic GVHD remains to be elucidated, especially in HLA-matched HCT with PTCY. Based on its safety profile, PTCY is currently applied for the human leucocyte antigen (HLA)-matched HCT setting. Here, we investigated the mechanisms of chronic GVHD following HLA-matched HCT with PTCY using a well-defined mouse chronic GVHD model. PTCY attenuated clinical and pathological chronic GVHD by suppressing effector T-cells and preserving regulatory T-cells compared with a control group. Additionally, we demonstrated that cyclosporine A (CsA) did not show any additional positive effects on attenuation of GVHD in PTCY-treated recipients. These results suggest that monotherapy with PTCY without CsA could be a promising strategy for the prevention of chronic GVHD following HLA-matched HCT. |
キーワード | GVHD posttransplant cyclophosphamide hematopoietic cell transplantation HLA-identical |
Amo Type | Original Article |
出版物タイトル | Acta Medica Okayama |
発行日 | 2024-04 |
巻 | 78巻 |
号 | 2号 |
出版者 | Okayama University Medical School |
開始ページ | 123 |
終了ページ | 134 |
ISSN | 0386-300X |
NCID | AA00508441 |
資料タイプ | 学術雑誌論文 |
言語 | 英語 |
著作権者 | Copyright Ⓒ 2024 by Okayama University Medical School |
論文のバージョン | publisher |
査読 | 有り |
PubMed ID | 38688830 |