Changes in proportion and function of peripheral CD4(+)LAP(+) regulatory T cells in children with asthma / 中国当代儿科杂志
Chinese Journal of Contemporary Pediatrics
;
(12): 726-730, 2016.
Artigo
em Chinês
| WPRIM
| ID: wpr-261158
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes in the proportion and function of peripheral CD4(+)LAP(+)regulatory T cells (CD4(+)LAP(+)Treg cells) in children with asthma, as well as the role of CD4(+)LAP(+)Treg cells in the pathogenesis of asthma.</p><p><b>METHODS</b>A total of 75 children who were diagnosed with asthma from March 2014 to September 2015 were enrolled as study subjects, and according to their conditions, they were divided into acute-stage asthma group (40 children) and remission-stage asthma group (35 patients). Another 30 children who underwent physical examination were enrolled as the healthy control group. Flow cytometry was used to determine the percentage of peripheral CD4(+)LAP(+)Treg cells, and [(3)H]-thymidine incorporation assay was performed to analyze the immunosuppression of CD4(+)LAP(+)Treg cells in each group.</p><p><b>RESULTS</b>The acute-stage asthma group showed significant reductions in the proportion of CD4(+)LAP(+)Treg cells compared with the remission-stage asthma group and the healthy control group (2.0%±1.0% vs 4.1%±2.4%/4.6%±3.0%; P<0.05). The acute-stage asthma group also showed a significant reduction in the immunosuppression rate of CD4(+)LAP(+)Treg cells compared with the remission-stage asthma group and the healthy control group (21%±4% vs 55%±9%/62%±11%; P<0.05).</p><p><b>CONCLUSIONS</b>In children with asthma, the reduction in the number and inhibitory function of peripheral CD4(+)LAP(+)Treg cells may be involved in the pathogenesis of asthma.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Asma
/
Linfócitos T Reguladores
/
Alergia e Imunologia
Limite:
Criança
/
Criança, pré-escolar
/
Feminino
/
Humanos
/
Masculino
Idioma:
Chinês
Revista:
Chinese Journal of Contemporary Pediatrics
Ano de publicação:
2016
Tipo de documento:
Artigo
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