2000 Fiscal Year Final Research Report Summary
Immunological control by the interaction between HLA-E and HLA-G in fetal-maternal interface
| Project/Area Number |
11671643
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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 | Nara Medical University |
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Principal Investigator |
ISHITANI Akiko Nara Medical University, Department of Legal Medicine, Assistant Professor, 医学部, 講師 (40112544)
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| Project Period (FY) |
1999 – 2000
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| Keywords | HLA-E / HLA-F / HLA-G / cytokine / signal peptide / placenta / trophoblast / NK receptor |
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| Research Abstract |
l) The effects of HLA-G expression of trophoblast cells on cytokine secretion by decidual mononuclea cells were examined. The HLA-G expression decreased the secretion of Th1-type cytokine, IFN γ and TNF α, and increased Th2-type cytokine, IL4 and IL10 suggesting that one of the main roles of HLA-G is to control cytokine network in placenta.
2) Although it had been thought that trophoblast cells expressed only HLA-G with neither any other class Ia nor class II HLA antigen, we showed HLA-E and HLA-F are also expressed on trophoblast using anti-HLA-E and anti-HLA-F monoclonal antibodies we had made.
3) Correlation between the expression of HLA-G and -E on trophoblasts and the cause of preeclampsia was examined. Several data were reported suggesting that one of the main causes of preeclampsia might bethe loss of the HLA-G expression on the trophoblasts. Although, we also found the partial lack of the expression of HLA-G on normal placenta . And those trophoblasts without the expression of HLA-G also did not express HLA-E, were surrounded with fiblin as same as trophoblasts of preeclampsia, and were not stained with eosin, suggesting that those cells were inert or dying already. That means the lack of expression of HLA-G on trophoblasts may be the result of the desease rather than the cause.
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