Impact and Modulations of Peripheral and Edaphic B Cell Subpopulations in Chronic Rhinosinusitis With Nasal Polyposis
Clinical and Experimental Otorhinolaryngology
;
: 133-140, 2018.
Article
Dans Anglais
| WPRIM
| ID: wpr-715064
ABSTRACT
OBJECTIVES:
The pathophysiological mechanisms of chronic rhinosinusitis with nasal polyposis (CRSwNP) still are discussed controversially. Regulatory B cells (Breg) are responsible for the suppression of T cell activity deficiencies for Breg have been demonstrated to contribute to autoimmune disorders, e.g., systemic lupus erythematosus. In order to evaluate the influence of B cell subpopulations, especially Breg, on the etiology of this disease, the aim of this study was to characterize subpopulations of peripheral and edaphic B cells in CRSwNP.METHODS:
Polypoid tissue and blood samples were collected from 10 patients undergoing paranasal sinus surgery and lymphocytes were analyzed by multicolor flow cytometry.RESULTS:
There was a significantly lower frequency of B cells in nasal polyps compared to peripheral blood mononuclear cells (PBMC) in patients with CRSwNP. Mature resting B cells were the main population within B cells in PBMC, and memory B cells in nasal polyps. Remarkably, Breg and mature B cells significantly decreased in nasal polyps compared to PBMC. Memory B cells significantly increased and represented the main subpopulation in nasal polyps in patients with CRSwNP.CONCLUSION:
In this study a detailed contemporary characterization of B cell subpopulations in patients with CRSwNP is presented. The influence of edaphic B cells could play a key role in the maintenance of this chronic infectious disease.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Plasmocytes
/
Lymphocytes B
/
Lymphocytes
/
Polypes du nez
/
Maladies transmissibles
/
Lymphocytes B régulateurs
/
Cytométrie en flux
/
Lupus érythémateux disséminé
/
Mémoire
Limites du sujet:
Humains
langue:
Anglais
Texte intégral:
Clinical and Experimental Otorhinolaryngology
Année:
2018
Type:
Article
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