Role of DcR3 in T Cell Activation in SLE and RA
1 other identifier
observational
450
1 country
1
Brief Summary
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.
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P75+ for all trials
Started Jan 2006
1 active site
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
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Study Timeline
Key milestones and dates
Study Start
First participant enrolled
January 1, 2006
CompletedFirst Submitted
Initial submission to the registry
January 11, 2006
CompletedFirst Posted
Study publicly available on registry
January 12, 2006
CompletedStudy Completion
Last participant's last visit for all outcomes
December 1, 2007
CompletedJanuary 12, 2006
December 1, 2005
January 11, 2006
January 11, 2006
Conditions
Eligibility Criteria
You may qualify if:
- SLE, RA
You may not qualify if:
- nil
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Study Sites (1)
National Taiwan University Hospital
Taipei, Taiwan
MeSH Terms
Conditions
Condition Hierarchy (Ancestors)
Study Officials
- PRINCIPAL INVESTIGATOR
Ping-Ning Hsu, MD, PhD
Department of Immunology
Central Study Contacts
Study Design
- Study Type
- observational
- Observational Model
- CASE CONTROL
- Time Perspective
- OTHER
- Sponsor Type
- OTHER
Study Record Dates
First Submitted
January 11, 2006
First Posted
January 12, 2006
Study Start
January 1, 2006
Study Completion
December 1, 2007
Last Updated
January 12, 2006
Record last verified: 2005-12