Yoshiyasu N, Sato M. Chronic lung allograft dysfunction post-lung transplantation: The era of bronchiolitis obliterans syndrome and restrictive allograft syndrome. World J Transplant 2020; 10(5): 104-116 [PMID: 32864356 DOI: 10.5500/wjt.v10.i5.104]
Corresponding Author of This Article
Masaaki Sato, MD, PhD, Director, Department of Thoracic Surgery, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. satom-sur@h.u-tokyo.ac.jp
Research Domain of This Article
Transplantation
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Transplant. May 29, 2020; 10(5): 104-116 Published online May 29, 2020. doi: 10.5500/wjt.v10.i5.104
Chronic lung allograft dysfunction post-lung transplantation: The era of bronchiolitis obliterans syndrome and restrictive allograft syndrome
Nobuyuki Yoshiyasu, Masaaki Sato
Nobuyuki Yoshiyasu, Masaaki Sato, Department of Thoracic Surgery, The University of Tokyo Hospital, Tokyo 113-8655, Japan
Author contributions: Yoshiyasu N and Sato M equally contributed to this paper in the conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Masaaki Sato, MD, PhD, Director, Department of Thoracic Surgery, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. satom-sur@h.u-tokyo.ac.jp
Received: February 24, 2020 Peer-review started: February 24, 2020 First decision: April 25, 2020 Revised: April 30, 2020 Accepted: May 12, 2020 Article in press: May 12, 2020 Published online: May 29, 2020 Processing time: 95 Days and 1.7 Hours
ARTICLE HIGHLIGHTS
Currently, CLAD is mainly classified into two clinical phenotypes, BOS and RAS. These mechanisms are not clear but considered to involve complex immune-mediated mechanisms such as innate immunity, cellular immunity, humoral immunity and autoimmunity. Finally, tissue remodeling takes place, resulting in irreversible fibrosis. An apparent histological difference between BOS and RAS is the anatomical locations involved: namely, BOS mainly involves small airways while peripheral lung tissue remains relatively intact, while RAS involves multiple anatomical compartments including airways, pleura, interlobular septum, alveoli, and vasculature. Such difference in the distribution of fibrosis may be associated with different magnitude and quality of immune mechanisms including lymphoid neogenesis.
