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Diminution of Circulating CD4+CD25 high T cells in naïve Crohn's disease.
Chamouard, Patrick; Monneaux, Fanny; Richert, Zoe; Voegeli, Anne-Claire; Lavaux, Thomas; Gaub, Marie Pierre; Baumann, René; Oudet, Pierre; Muller, Sylviane.
Afiliação
  • Chamouard P; Service d'Hépato-Gastroentérologie et d'Assistance Nutritive, Hôpital de Hautepierre, 67098 Strasbourg Cedex, France. Patrick.Chamouard@chru-strasbourg.fr
Dig Dis Sci ; 54(10): 2084-93, 2009 Oct.
Article em En | MEDLINE | ID: mdl-19051021
ABSTRACT
Crohn's disease is considered to be caused either by an excess of T-cell effector functions and/or by a defective regulatory T-cell compartment. The aim of this study was to assess in Crohn's disease the frequency of circulating CD4(+)CD25(high) T cells that possess regulatory T-cell functions and CD4(+)CD25(low) T cells that contain activated T cells. Flow cytometry of peripheral blood was used to assess CD4(+)CD25(high) and CD4(+)CD25(low) T-cell frequencies in a cohort of 66 patients with Crohn's disease in comparison to 19 patients with ulcerative colitis and 31 healthy individuals enrolled as controls. The CD4(+)CD25(high) T-cell frequency was significantly lowered in naïve Crohn's disease (P = 0.013) and in ulcerative colitis (P = 0.001). CD4(+)CD25(low) T-cell frequency was increased in Crohn's disease (P = 0.0001) and in ulcerative colitis (P = 0.0002). Both CD4(+)CD25(high) and CD4(+)CD25(low) T-cell frequencies are altered in naïve Crohn's disease resulting in an imbalance between both populations and a relative contraction of the CD4(+)CD25(high) T-cell population.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doença de Crohn / Antígenos CD4 / Linfócitos T Reguladores / Subunidade alfa de Receptor de Interleucina-2 Idioma: En Ano de publicação: 2009 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doença de Crohn / Antígenos CD4 / Linfócitos T Reguladores / Subunidade alfa de Receptor de Interleucina-2 Idioma: En Ano de publicação: 2009 Tipo de documento: Article