| The role of Foxp3+ regulatory T-cells in endometriosis: a potential controlling mechanism for a complex, chronic immunological condition. | |
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MedLine Citation:
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PMID: 20150173 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Endometriosis is an inflammatory condition, associated with highly dysregulated immune response at both uterine and peritoneal levels. Surprisingly, Foxp3+ regulatory T-cells, which control and suppress a range of immune responses, have not previously been investigated in endometriosis. METHODS AND RESULTS: Immunohistochemical analysis of Foxp3+ cells in 127 eutopic endometrial samples and 59 ectopic peritoneal lesions revealed that these immune cell populations are highly disturbed in women suffering from endometriosis. We showed that Foxp3+ cells remained highly up-regulated during the secretory phase of the menstrual cycle, while at this time their expression is significantly down-regulated in women without endometriosis (P < 0.001). Foxp3+ cells were detected in the stroma of 18 of the 59 peritoneal endometriotic lesions, but not in the surrounding or control peritoneal tissue. CONCLUSIONS: We propose that in eutopic endometrium in women with endometriosis Foxp3+ cells decrease the ability of newly recruited immune cell populations to effectively recognize and target endometrial antigens shed during menstruation, allowing their survival and ability to implant in ectopic sites. At these ectopic sites, variable expression of Foxp3+ cells within some peritoneal endometriotic lesions is likely to be linked to the characteristics and stage of individual lesion development and be playing key roles in pathogenesis and progression of this unique condition. |
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Authors:
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Marina Berbic; Alison J Hey-Cunningham; Cecilia Ng; Natsuko Tokushige; Subha Ganewatta; Robert Markham; Peter Russell; Ian S Fraser |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-02-10 |
Journal Detail:
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Title: Human reproduction (Oxford, England) Volume: 25 ISSN: 1460-2350 ISO Abbreviation: Hum. Reprod. Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-17 Completed Date: 2010-06-17 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8701199 Medline TA: Hum Reprod Country: England |
Other Details:
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Languages: eng Pagination: 900-7 Citation Subset: IM |
Affiliation:
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Department of Obstetrics and Gynaecology, Queen Elizabeth II Research Institute for Mothers and Infants, the University of Sydney, New South Wales, Australia. m.berbic@usyd.edu.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Case-Control Studies Endometriosis / immunology*, metabolism, pathology Female Forkhead Transcription Factors / immunology*, metabolism* Humans Immunohistochemistry Menstrual Cycle / immunology, metabolism Middle Aged Peritoneal Diseases / immunology, metabolism, pathology Peritoneum / cytology, immunology, metabolism T-Lymphocytes, Regulatory / immunology*, metabolism*, pathology Young Adult |
| Chemical | |
Reg. No./Substance:
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0/FOXP3 protein, human; 0/Forkhead Transcription Factors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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