Endometriosis is a common and puzzling gynaecological condition which shows a great deal of variability between women. It affects up to 15% of all women of reproductive age. There is a strong familial component, but the aetiology and pathogenesis are still uncertain. Endometriosis is an 'inflammatory' condition with substantial numbers of leukocytes recruited into the lesion sites. There is increasing evidence to demonstrate marked changes in numbers and functions of these leukocytes in the eutopic endometrium and peritoneal fluid as well as in the lesions. We hypothesise that endometriosis is primarily an endometrial disease with underlying genetic disturbances which lead to a number of major molecular changes in function, enhancing the likelihood that viable fragments of endometrial tissue will pass through the fallopian tubes and attach and grow on the peritoneum. We have demonstrated disturbances in the populations of T cells, B cells, mast cells, dendritic cells and macrophages within the endometrium and ectopic lesions, and are intrigued by the potential for changes in regulatory T cells to influence disease establishment and progression. Interestingly, we have shown that in endometriosis, naturally occurring FOXP3+ regulatory T cells fail to undergo the expected decline in number during the secretory phase, which may account for a decreased ability of newly recruited leukocytes to initiate effective immune responses against viable endometrial fragments, permitting their survival and subsequent establishment. To better understand the pathogenesis of endometriosis, we must learn about how the immune system recognises this disease and how the endometrial immune response is regulated.
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