The prevalence of Th17 cells in patients with acute myeloid leukemia / 中华血液学杂志
Chinese Journal of Hematology
; (12): 617-620, 2010.
Article
em Zh
| WPRIM
| ID: wpr-353604
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the proportion of Th17 cells in the peripheral blood of the patients with acute myeloid leukemia (AML) and evaluate the potential association of Th17 cells with AML.</p><p><b>METHODS</b>The cytokines IL-17 and TGF-β1 in the peripheral blood of AML patients before therapy (group 1), AML patients in complete remission (AML-CR, group 2) and healthy donors (group 3) were measured by enzyme-linked immunosorbent assay (ELISA). The proportion of Th17 cells of each group was evaluated by flow cytometry. The level of IL-17 mRNA of each group was examined by reverse transcription-PCR (RT-PCR).</p><p><b>RESULTS</b>The percentage of Th17 cells and the level of IL-17, IL-17 mRNA in group 1 \[(10.502 ± 1.071) ng/L, (0.935 ± 0.140)% and 0.262 ± 0.510\] and group 2 \[(11.345 ± 0.987) ng/L, (1.091 ± 0.159)% and 0.307 ± 0.031\] was significantly lower than that in group 3 \[(16.852 ± 1.198) ng/L, (2.586 ± 0.235)% and 0.501 ± 0.060\]. The percentage of Th17 cells and the level of IL-17, IL-17 mRNA in group 1 was lower than that in the group 2. But the level of TGF-β1 in the group 1 (29.963 ± 1.588) ng/L and the group 2 (25.163 ± 1.848) ng/L was significantly higher than that in group 3 (13.366 ± 1.565) ng/L. However, the level of TGF-β1 in the group 3 was higher than that of the group 2.</p><p><b>CONCLUSION</b>Th17 cells might be negatively correlated with the AML development. The overexpression of TGF-β1 in AML patients might suppress the differentiation of Th17 cells.</p>
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Ensaio de Imunoadsorção Enzimática
/
Leucemia Mieloide Aguda
/
Prevalência
/
Interleucina-17
/
Fator de Crescimento Transformador beta1
/
Células Th17
Tipo de estudo:
Prevalence_studies
Limite:
Humans
Idioma:
Zh
Revista:
Chinese Journal of Hematology
Ano de publicação:
2010
Tipo de documento:
Article