Premature Immunosenescence Impairs Immune Surveillance Allowing the Endometriotic Stem Cell to Migrate: The Cytokine Profile as a Common Denominator

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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 immunosenescent states and in conditions with reduced immune surveillance, while the same variations are recorded in endometriotic patients. It is probable that these are common to all process signals, guide the endometriotic stem cell and dictate its fate according to the stochastic, transdifferentiation (plasticity) or deterministic model to become capable of migration and tissue invasion. It is currently unknown whether the pathway taken by the hemopoietic stem cell to become endometriotic represents a normal or aberrant route of development. This prompts research into its isolation and in vitro study of its behavior in order to reveal its potential function and role in endometriosis. (Journal of Endometriosis 2010; 2: 7–18)