| Project/Area Number |
15591772
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | KYOTO PREFECTURAL UNIVERSITY OF MEDICINE |
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Principal Investigator |
KITAWAKI Jo Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Associate Professor, 医学研究科, 助教授 (00204925)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | ENDOMETRIOSIS / POLYMORPHISMS / CYTOKINES / TNF-α / INTERFERON-γ / HLA |
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| Research Abstract |
Endometriosis is defined by the presence of endometrium-like lesions outside the uterine cavity. Although the exact etiology and pathogenesis are unclear, genetic, endocrine, immune, and environment factors have been implicated in the disease. Familial and twin studies have indicated 5-8% increase in risk for first-degree relatives, suggesting that endometriosis is a genetic disorder with polygenic or multifactorial inheritance. Studies have implied a role for genetic factors in the association between the development of endometriosis and genetic polymorphisms.
Defects in the ability of cytotoxic T cells and natural killer (NK) cells to recognize and lyse ectopic endometrial cells are considered crucial for disease pathogenesis. NK cells recognize specifically the HLA class I molecules that inhibit the killing functions of these T cells. In the present study, we found that the HLA-A24-B^*0702-Cw^*0702-DRB1^*0101 haplotype and polymorphisms in the TNF-α gene promoter and interferon-γ gene are possible genetic susceptibility factors. Interleukin-10 gene promoter polymorphism is associated with production of anti-carbonic anhydrase II autoantibodies in patients with endometriosis.
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