Loss of stromal cell Thy-1 plays a critical role in lipopolysaccharide induced chronic lung allograft dysfunction.
Thy-1
bronchiolitis
clad
fibroblasts
fibrosis
Journal
The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
received:
17
05
2021
revised:
14
04
2022
accepted:
12
05
2022
pubmed:
13
6
2022
medline:
28
7
2022
entrez:
12
6
2022
Statut:
ppublish
Résumé
Long-term survival of lung transplants lags behind other solid organs due to early onset of a fibrotic form of chronic rejection known as chronic lung allograft dysfunction (CLAD). Preventing CLAD is difficult as multiple immunologic and physiologic insults contribute to its development. Targeting fibroblast activation, which is the final common pathway leading to CLAD, offers the opportunity to ameliorate fibrosis irrespective of the initiating insult. Thy-1 is a surface glycoprotein that controls fibroblast differentiation and activation. To study the role of Thy-1 in CLAD, we utilized the minor antigen mismatched C57BL/6 (B6 More severe CLAD was evident in B6 Our findings suggest that the loss of Thy-1 on fibroblasts is a previously unrecognized cause of CLAD and its replacement may offer therapeutic applications for amelioration of this disease post-transplantation in the setting of infectious stress responses.
Sections du résumé
BACKGROUND
Long-term survival of lung transplants lags behind other solid organs due to early onset of a fibrotic form of chronic rejection known as chronic lung allograft dysfunction (CLAD). Preventing CLAD is difficult as multiple immunologic and physiologic insults contribute to its development. Targeting fibroblast activation, which is the final common pathway leading to CLAD, offers the opportunity to ameliorate fibrosis irrespective of the initiating insult. Thy-1 is a surface glycoprotein that controls fibroblast differentiation and activation.
METHODS
To study the role of Thy-1 in CLAD, we utilized the minor antigen mismatched C57BL/6 (B6
RESULTS
More severe CLAD was evident in B6
CONCLUSIONS
Our findings suggest that the loss of Thy-1 on fibroblasts is a previously unrecognized cause of CLAD and its replacement may offer therapeutic applications for amelioration of this disease post-transplantation in the setting of infectious stress responses.
Identifiants
pubmed: 35691796
pii: S1053-2498(22)01946-5
doi: 10.1016/j.healun.2022.05.009
pii:
doi:
Substances chimiques
Lipopolysaccharides
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1044-1054Subventions
Organisme : NIAID NIH HHS
ID : P01 AI116501
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI145108
Pays : United States
Informations de copyright
Published by Elsevier Inc.