The Role of CD4(+)CD25(bright) Regulatory T Cells in the Maintenance of Pregnancy, Premature Rupture of Membranes, and Labor
Yonsei Medical Journal
;
: 366-371, 2008.
Artigo
em Inglês
| WPRIM
| ID: wpr-79518
ABSTRACT
PURPOSE:
The aim of this study was to evaluate the changes of the regulatory T cell subset in peripheral blood caused by gestational age and premature rupture of membranes (PROM) with or without labor to verify the role of regulatory T cells in pregnancy. PATIENTS ANDMETHODS:
We investigated regulatory T cell distribution in the peripheral blood of pregnancies during the first trimester (group I, n=2), the second trimester (group II, n=12), and the third trimester without PROM and labor (group III, n=15). In addition, we evaluated pregnancies in the third trimester complicated by PROM (group IV, n=4) and labor with no complication by PROM (Group V, n=5). Comparisons were made with non-pregnant controls (group VI, n=4) using flow cytometry.RESULTS:
During uncomplicated pregnancy, the CD4(+)CD25(bright) regulatory T cell population decreased with advancing gestational age (group I=3.35+/-0.47, group II=2.91+/-1.44, group III=2.81+/-1.36, group VI=2.52+/-0.71, p=NS). When we compared group IV with group III and V to evaluate the changes of the regulatory T cells with PROM, the CD4(+)CD25(bright) regulatory T cell population was significantly decreased in group IV compared to group III (p=0.001) and group V (p=0.026).CONCLUSION:
The present results revealed that the regulatory T cell population increased in early pregnancy but decreased in pregnancies complicated by PROM, indicating that regulatory T cells might be related to the maintenance of pregnancy.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Ruptura Prematura de Membranas Fetais
/
Trabalho de Parto
/
Antígenos CD4
/
Idade Gestacional
/
Linfócitos T Reguladores
/
Subunidade alfa de Receptor de Interleucina-2
Limite:
Feminino
/
Humanos
/
Gravidez
Idioma:
Inglês
Revista:
Yonsei Medical Journal
Ano de publicação:
2008
Tipo de documento:
Artigo
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