The Association of Costimulatory Molecules and PPAR-polymorphisms With Autoimmune Thyroid Disease in Taiwan
NCT01260532 · Status: UNKNOWN · Type: OBSERVATIONAL · Enrollment: 300
Last updated 2010-12-15
Summary
Autoimmune thyroid disease is the most common organ-specific autoimmune disease. AITD include Graves' disease and Hashimoto's thyroiditis. Although the pathogenesis of AITD remains unclear, it is generally thought that the mechanisms of the disease is a complex disease in which susceptibility genes and environmental triggers act in concert to initiate the autoimmune response to the thyroid.
The initial step of thyroid autoimmunity is the activation of T cells. The activation of T cell requires two signals: firstly, thyroid follicular cells or antigen presenting cells binds to T cell receptor through antigenic HLA complex. Secondly, the activation of T cells is also required the interaction of costimulatory molecules between thyroid follicular cells and immune cells, including CTLA-4, CD 40, CD28, ICOS. PPAR- is a kind of intranuclear transcription factor, associated with adipogenesis and inflammation. Some reports showed that PPAR- polymorphism may have a protective effect from Graves' ophthalmopathy.
The goal of the study is to investigate the relationship among SNP and mRNA of costimulatory molecules and PPAR- , serum cytokine including TNF- and sIL-2R, and clinical characteristics in AITD patients. From the study, we hope to clarify the role of costimulatory molecules and PPAR- polymorphism in AITD.
Conditions
- AITd Patients With Different Polymorphisms
Sponsors & Collaborators
-
Taipei Medical University WanFang Hospital
lead OTHER
Principal Investigators
-
Jiunn-Diann Lin · Taipei Medical University WanFang Hospital
Eligibility
- Min Age
- 20 Years
- Sex
- ALL
- Healthy Volunteers
- No
Timeline & Regulatory
- Start
- 2009-07-31
- Completion
- 2019-06-30
Countries
- Taiwan
Study Locations
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