Semaphorin 7A is expressed on airway ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Semaphorin 7A is expressed on airway eosinophils and upregulated by IL-5 family cytokines.
Auteur(s) :
Esnault, Stéphane [Auteur]
University of Wisconsin School of Medicine and Public Health
Kelly, Elizabeth A [Auteur]
University of Wisconsin School of Medicine and Public Health
Johansson, Mats W [Auteur]
University of Wisconsin School of Medicine and Public Health
Liu, Lin Ying [Auteur]
University of Wisconsin School of Medicine and Public Health
Han, Shih-Tsung [Auteur]
University of Wisconsin School of Medicine and Public Health
Akhtar, Moneeb [Auteur]
University of Wisconsin School of Medicine and Public Health
Sandbo, Nathan [Auteur]
University of Wisconsin School of Medicine and Public Health
Mosher, Deane F [Auteur]
University of Wisconsin School of Medicine and Public Health
Denlinger, Loren C [Auteur]
University of Wisconsin School of Medicine and Public Health
Mathur, Sameer K [Auteur]
University of Wisconsin School of Medicine and Public Health
Malter, James S [Auteur]
University of Texas Southwestern Medical Center [Dallas]
Jarjour, Nizar N [Auteur]
University of Wisconsin School of Medicine and Public Health
University of Wisconsin School of Medicine and Public Health
Kelly, Elizabeth A [Auteur]
University of Wisconsin School of Medicine and Public Health
Johansson, Mats W [Auteur]
University of Wisconsin School of Medicine and Public Health
Liu, Lin Ying [Auteur]
University of Wisconsin School of Medicine and Public Health
Han, Shih-Tsung [Auteur]
University of Wisconsin School of Medicine and Public Health
Akhtar, Moneeb [Auteur]
University of Wisconsin School of Medicine and Public Health
Sandbo, Nathan [Auteur]
University of Wisconsin School of Medicine and Public Health
Mosher, Deane F [Auteur]
University of Wisconsin School of Medicine and Public Health
Denlinger, Loren C [Auteur]
University of Wisconsin School of Medicine and Public Health
Mathur, Sameer K [Auteur]
University of Wisconsin School of Medicine and Public Health
Malter, James S [Auteur]
University of Texas Southwestern Medical Center [Dallas]
Jarjour, Nizar N [Auteur]
University of Wisconsin School of Medicine and Public Health
Titre de la revue :
Clinical Immunology
Nom court de la revue :
Clin Immunol
Numéro :
150
Pagination :
90-100
Date de publication :
2014-01-01
ISSN :
1521-7035
Mot(s)-clé(s) en anglais :
Actins
Allergens
Antigens, CD
Bronchoalveolar Lavage Fluid
CD4-Positive T-Lymphocytes
Cells, Cultured
Eosinophils
Fibroblasts
GPI-Linked Proteins
Humans
Hypersensitivity
Interleukin-5
Lung
Semaphorins
Up-Regulation
BAL
EOS
Eosinophil
Fibrosis
IL-3
RT-qPCR
SBP-Ag
Sema7a
Semaphorin 7A
Translation
bronchoalveolar lavage
eosinophils
real-time quantitative PCR
segmental bronchoprovocation with allergen
semaphorin 7A.
Allergens
Antigens, CD
Bronchoalveolar Lavage Fluid
CD4-Positive T-Lymphocytes
Cells, Cultured
Eosinophils
Fibroblasts
GPI-Linked Proteins
Humans
Hypersensitivity
Interleukin-5
Lung
Semaphorins
Up-Regulation
BAL
EOS
Eosinophil
Fibrosis
IL-3
RT-qPCR
SBP-Ag
Sema7a
Semaphorin 7A
Translation
bronchoalveolar lavage
eosinophils
real-time quantitative PCR
segmental bronchoprovocation with allergen
semaphorin 7A.
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may ...
Lire la suite >Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may be a significant source of sema7a. In vivo, sema7a was expressed on the surface of circulating eosinophils and upregulated on bronchoalveolar lavage eosinophils obtained after segmental bronchoprovocation with allergen. Based on mRNA levels in unfractionated and isolated bronchoalveolar cells, eosinophils are the predominant source of sema7a. In vitro, among the members of the IL-5-family cytokines, sema7a protein on the surface of blood eosinophils was increased more by IL-3 than by GM-CSF or IL-5. Cytokine-induced expression of cell surface sema7a required translation of newly synthesized protein. Finally, a recombinant sema7a induced alpha-smooth muscle actin production in human bronchial fibroblasts. semaphorin 7A is a potentially important modulator of eosinophil profibrotic functions in the airway remodeling of patients with chronic asthma.Lire moins >
Lire la suite >Semaphorin 7A (sema7a) plays a major role in TGF-β1-induced lung fibrosis. Based on the accumulating evidence that eosinophils contribute to fibrosis/remodeling in the airway, we hypothesized that airway eosinophils may be a significant source of sema7a. In vivo, sema7a was expressed on the surface of circulating eosinophils and upregulated on bronchoalveolar lavage eosinophils obtained after segmental bronchoprovocation with allergen. Based on mRNA levels in unfractionated and isolated bronchoalveolar cells, eosinophils are the predominant source of sema7a. In vitro, among the members of the IL-5-family cytokines, sema7a protein on the surface of blood eosinophils was increased more by IL-3 than by GM-CSF or IL-5. Cytokine-induced expression of cell surface sema7a required translation of newly synthesized protein. Finally, a recombinant sema7a induced alpha-smooth muscle actin production in human bronchial fibroblasts. semaphorin 7A is a potentially important modulator of eosinophil profibrotic functions in the airway remodeling of patients with chronic asthma.Lire moins >
Langue :
Anglais
Comité de lecture :
Oui
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Université de Lille
Inserm
CHU Lille
Inserm
CHU Lille
Collections :
Date de dépôt :
2023-11-10T15:25:05Z
2024-03-16T08:30:54Z
2024-03-16T08:30:54Z
Fichiers
- SEMA7A on EOS 2014.pdf
- Version éditeur
- Accès restreint
- Accéder au document