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临床试验/NCT00452764
NCT00452764已完成不适用

Phenotype and Number of Regulatory T Cells Present in Peripheral Blood of COPD Patients Versus Healthy Controls

Groningen Research Institute for Asthma and COPD1 个研究点 分布在 1 个国家目标入组 50 人开始时间: 2007年1月最近更新:
适应症

试验速览

阶段
不适用
状态
已完成
发起方
入组人数
50
试验地点
1

研究概览

简要总结

Lymphoid follicles, consisting of T-and B cells, are involved in the chronic inflammatory response in COPD. Foxp3 positive regulatory T cells (Tregs) are present in these follicles and may be involved in the suppression of this chronic inflammatory response.

We hypothesise that a dysfunction of Tregs underlies the development of the inflammatory response in COPD. This could be either due to a decreased presence of Tregs in COPD, or to an altered function of Tregs possibly caused by a decreased HO-1 expression and/or an altered TGFβ regulation.

详细描述

COPD is a leading cause of death worldwide and its morbidity and mortality are still rising.So far, no effective treatment is available To find better treatment methods more insight is needed in the nature/origin of the chronic inflammation that underlies the development of COPD.

The important role of neutrophils, macrophages and cytotoxic T cells is well established in this respect, yet the role of CD4 T cells and B cells has only recently (re)attracted attention. We detected the presence of lymphoid follicles in lung tissue of COPD patients, consisting of B cells surrounded by T cells. Recently, we have found the presence of Foxp3 positive T cells as a component of these lymphoid follicles in COPD. Since Foxp3 is a distinctive marker of regulatory T cells (Tregs), this finding suggests that Tregs are involved in the inflammatory response in COPD.

Tregs are important in controlling immunological tolerance and preventing auto-immune responses by inhibiting T-cell responses. Dysfunction of Tregs can lead to auto-immune diseases, allergy and chronic inflammatory diseases. However, nothing is known so far about their contribution to the chronic inflammatory response in COPD. Recent studies show that, next to direct inhibition by cell-cell contact, the inhibitory effects of Tregs are mediated by heme oxygenase-1 (HO-1) expression and membrane bound TGFβ.

We hypothesise that a dysfunction of regulatory T cells underlies the development of the inflammatory response in COPD. This could be due to a decreased presence of Tregs in COPD, or to an altered function of Tregs. The latter may be due to a decreased HO-1 expression, as we have shown in macrophages of COPD patients compared to those in healthy controls, and/or an altered TGFβ regulation, a cytokine that plays a prime role in COPD.

研究设计

研究类型
Observational
时间视角
Prospective

入排标准

年龄范围
40 Years 至 —(Adult, Older Adult)
性别
Male
接受健康志愿者

入选标准

  • COPD patients
  • Clinical diagnosed COPD
  • No allergies
  • Post-bronchodilator FEV1 < 80% predicted, and post-bronchodilator FEV1/FVC < 70%
  • No use of (inhaled) corticosteroids in the 6 weeks preceding the study
  • Age > 40
  • Smokers and ex- smokers > 10 pack years
  • Ex-smokers have to have quitted smoking for at least one year
  • No other major current health problems
  • Informed consent Healthy controls
  • No signs of pulmonary disease
  • No allergies or hyperreactivity
  • No other major current health problems
  • FEV1 > 90 % predicted, FEV1/FVC > 70%
  • Age > 40
  • Never smokers, i.e. no cigarettes last year, and maximal 5 pack years
  • Smokers and ex- smokers > 10 pack years
  • Ex-smokers have to have quitted smoking for at least one year
  • Informed consent

排除标准

  • Use of (inhaled) corticosteroids in the 6 weeks preceding the study
  • Addiction to alcohol or drugs
  • COPD exacerbation in the 6 weeks preceding the study

研究者

发起方
Groningen Research Institute for Asthma and COPD
申办方类型
Other

研究点 (1)

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