Evaluation of the frequency of invariant natural killer T (iNKT) cells in nasal polyps.
Adolescent
Adult
Chronic Disease
Female
Genes, T-Cell Receptor beta
/ genetics
Humans
Immunoglobulin E
/ metabolism
Leukocyte Count
Leukocytes, Mononuclear
Male
Middle Aged
Nasal Polyps
/ genetics
Natural Killer T-Cells
/ pathology
Receptors, Antigen, T-Cell
/ genetics
Rhinitis
/ genetics
Sinusitis
/ genetics
Young Adult
Flow cytometry
Invariant natural killer T-cells
NKT
Nasal polyp
Th2
Journal
Clinical immunology (Orlando, Fla.)
ISSN: 1521-7035
Titre abrégé: Clin Immunol
Pays: United States
ID NLM: 100883537
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
received:
15
10
2018
revised:
19
04
2019
accepted:
28
05
2019
pubmed:
4
6
2019
medline:
21
4
2020
entrez:
2
6
2019
Statut:
ppublish
Résumé
Nasal polyps (NP) are associated with inflamed mucosa of unknown etiology. The role of T cells in nasal polyposis is unclear. Invariant natural killer T cells (iNKT) can promote Th2 responses and have been implicated in some types of asthma. As there are shared inflammatory pathways involved in asthma and NPs, we evaluated the frequency of iNKT in 17 patients with NPs, but without asthma. A median of 6% polyp cells were T lymphocytes, of which iNKT were 0 to 2.38% (mean 0.674%). In the matched group (n = 10), iNKT in NPs was significantly higher than PBMCs (1.057% vs 0.155%, P < 0.05). Relative expression of Vα24 to TCR-beta genes in polyps (n = 14) was higher than blood in matched samples (n = 4). The presence of greater proportions of iNKT in NPs than in blood suggests that iNKT may play a role in the pathogenesis of nasal polyposis.
Identifiants
pubmed: 31152891
pii: S1521-6616(18)30619-3
doi: 10.1016/j.clim.2019.05.013
pii:
doi:
Substances chimiques
Receptors, Antigen, T-Cell
0
Valpha24 protein, human
0
Immunoglobulin E
37341-29-0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
125-129Informations de copyright
Copyright © 2019. Published by Elsevier Inc.