Abstract
While endometriosis, one of the most common reasons for infertility, remains a multifactorial condition and its exact cause highly speculative, there are data pointing to novel pathways of disease initiation which involve a stem cell and its ability to migrate and implant after it differentiates into an endometriotic stem cell. Thus, the mechanisms conferring immune surveillance, which would also normally expel the mesenchymal endometriotic cell, impairing its migration and implantation, appear to be negatively influenced by a state of endometriotic premature immunosenescence. This interplay between the two immunological mechanisms and endometriosis is influenced by a number of common factors having an active role in the host's protection process that inhibits harmful diseases and maintains cellular homeostasis. It appears more than coincidental that production/inhibition of IFN-γ, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-15, IL-18, TNF-α, VEGF, ICAM-1, and the number of Tolllike receptors is the same in ...
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