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Role of DcR3 in T Cell Activation in SLE and RA

The recruitment status of this study is unknown because the information has not been verified recently.
Verified December 2005 by National Taiwan University Hospital.
Recruitment status was  Recruiting
Sponsor:
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00275899
First received: January 11, 2006
Last updated: NA
Last verified: December 2005
History: No changes posted

January 11, 2006
January 11, 2006
January 2006
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No Changes Posted
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Role of DcR3 in T Cell Activation in SLE and RA
Role of DcR3 in T Cell Activation in SLE and RA

Decoy receptor 3 (DcR3), a new member of tumor necrosis factor receptor (TNFR) superfamily, is a decoy receptor for FasL and could inhibit FasL-induced apoptosis, has recently been shown to induce costimulation of T cells. Systemic lupus erythematosus (SLE) is an autoimmune disease with pathogenic autoantibodies and immune complexes results from abnormal immune responses including T and B lymphocyte hyperactivity, and formation of pathogenic subsets of autoantibodies. Rhematoid arthritis (RA) is a multi-systemic autoimmune disease characterized by persistent inflammatory synovitis. Activated T lymphocytes infiltration to synovium is strongly correlated with the symptoms. DcR3 mRNA is expressed in peripheral-blood T cells and is up-regulated after antigenic stimulation. The DcR3 gene has been demonstrated to be overexpressed in patients with sclerosis or SLE; however, role of DcR3 in SLE and RA as well as the effects of DcR3 on T cell immune response is still not clear. This study is to investigate role of DcR3-induced T cell activation in SLE and RA. The genetic polymorphisms of DcR3 in association with SLE and RA will be studied to elucidate the genetic factors associated with development of SLE and RA. For further explore the possible molecular mechanisms of elevated DcR3 in association with SLE, we attempt to study whether DcR3 could induce T cell activation via costimualtion and/or inhibit the activation induced cell death (AICD) of activated T cells in SLE and RA. This study will provide a new direction of therapy in reverse T cell hyper-reactivity in SLE and RA.

Specific Aim 1. Study DcR3-induced T cell activation in SLE and RA. A. Patients and controls Patients with SLE and RA in Department of Internal Medicine, National Taiwan University Hospital will be studied. All patient meet the criteria of the American College of Rheumatologists for diagnosis of SLE and RA. As controls, 20 healthy age- and gender-matched volunteers will be used. All the studies including samples involving human is in accordance with institutional guidelines.

B. Detection of serum DcR3 protein in SLE and RA patients C. T cell proliferation assay

Specific Aim 2. Study effects of DcR3 on activation-induced cell death (AICD) in SLE and RA In order to understand whether DcR3 could reduce the AICD in activated T cells in SLE and RA patients, the T cells from these patients will be assayed their AICD in the presence and absence of soluble DcR3-Fc.

Specific Aim 3. To investigate the association of clinical manifestation of SLE and RA with genetic polymorphism on DcR3 genes.

A. The gene sequencing and single nucleotide polymorphism (SNP) analysis of DcR3 genes.

B. The association of clinical manifestation of SLE and RA with genetic polymorphism on DcR3 genes.

Observational
Observational Model: Case Control
Primary Purpose: Screening
Time Perspective: Cross-Sectional
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  • SLE
  • Rheumatoid Arthritis
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Recruiting
450
December 2007
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Inclusion Criteria:

  • SLE, RA

Exclusion Criteria:

  • nil
Both
18 Years and older
Yes
Contact: Ping-Ning Hsu, PhD 886-2-23123456 ext 8635 phsu@ha.mc.ntu.edu.tw
Taiwan
 
NCT00275899
9461701220
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National Taiwan University Hospital
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Principal Investigator: Ping-Ning Hsu, MD, PhD Department of Immunology
National Taiwan University Hospital
December 2005

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP