Decreased expression of transmembrane TNFR2 in lung leukocytes subpopulations of patients with non-fibrotic hypersensitivity pneumonitis compared with the fibrotic disease

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Détails bibliographiques
Publié dans:Clinical immunology (Orlando, Fla.). - 1999. - 215(2020) vom: 01. Juni, Seite 108424
Auteur principal: Chavez-Galan, Leslie (Auteur)
Autres auteurs: Buendia-Roldan, Ivette, Castillo-Castillo, Kelly, Preciado-Garcia, Mario, Ocaña-Guzmán, Ranferi, Salgado, Alfonso, Gaxiola, Miguel, Selman, Moises
Format: Article en ligne
Langue:English
Publié: 2020
Accès à la collection:Clinical immunology (Orlando, Fla.)
Sujets:Journal Article Hypersensitivity pneumonitis Myeloid cells TNF TNFRs CD3 Complex Interleukin-8 Membrane Proteins Receptors, Tumor Necrosis Factor, Type I Receptors, Tumor Necrosis Factor, Type II Tumor Necrosis Factor-alpha
Description
Résumé:Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
Hypersensitivity pneumonitis (HP) is an interstitial lung disease, characterized by lung inflammation (non-fibrotic HP) that may often progresses to fibrosis (Fibrotic HP). The tumor necrosis factor (TNF) and its receptors (TNFR1 and TNFR2) can be found as soluble (sol) and transmembrane (tm) forms, playing pro-inflammatory functions but also has been related to immune regulatory functions. Bronchioalveolar lavage from fibrotic and non-fibrotic HP patients was obtained, and immune cells were characterized by flow cytometry, whereas soluble proteins were analyzed by ELISA. Compare to fibrotic HP patients, HP patients with non-fibrotic disease have accumulation of pro-inflammatory CD3+ myeloid cells, cell subpopulations that have decreased tmTNFR2 expression, and low frequency of regulatory-T cells. Whereas solTNF, solTNFR2, and IL-8 are increased. These findings suggest that the TNF pathway may explain, at least partially, the differences between both HP clinical forms. The evaluation of the TNF family molecules may help to develop new therapeutic approaches
Description:Date Completed 29.01.2021
Date Revised 29.01.2021
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2020.108424