**1. Introduction**

Endometriosis is a common gynecological disorder affecting ca. 10% women of reproductive age. The disease is related to the endometrial-like tissue (endometrial glands and stroma) located outside the uterine cavity, mainly on the pelvic viscera and/or ovaries. Endometriosis is associated with chronic pelvic inflammation and manifests with dysmenorrhea, dyspareunia or chronic pelvic pain. It also accounts for ca. 50% of women's infertility. Endometriosis is a debilitating disorder having a significant impact on patients' quality of life. Nevertheless, the etiopathogenesis of this disease is still poorly understood [1–4].

There are several theories on the origin of the endometriosis; however, the most accepted cause of this disease is retrograde menstrual blood flow [5]. In this mechanism shed endometrial cells enter the peritoneal cavity, where they survive and form ectopic foci of the endometriotic tissue. This may be possible owing to the resistance of endometriotic cells to apoptosis and their increased adhesiveness and invasiveness [6–9]. It is also plausible that the formation of ectopic endometriotic lesions may also be facilitated by a permissive local peritoneal milieu as well as abrogated elimination of endometriotic cells by the cells of the local immune system, e.g., NK cells and macrophages [10,11].

Due to chronic pelvic inflammation and the elevated production of a variety of autoantibodies such as anti-nuclear, anti-phospholipid, and anti-endometrial antibodies, endometriosis may be considered as an autoimmune/autoinflammatory disorder [11–14]. The disease manifests with the local and systemic abnormal lymphocyte responses and abrogated NK cell cytotoxicity [10,13,15–17]. Pelvic inflammation includes peritoneal infiltration with a variety of immune cells including various subsets of lymphocytes, activated macrophages and granulocytes [18,19]. The endometriotic peritoneal milieu is also characterized by a local excessive production and accumulation of a bulk of proinflammatory and regulatory cytokines [20,21].

The role of the peritoneal milieu and the peritoneal fluid (PF) in the immunopathogenesis of endometriosis still remains obscure. Although endometriosis is considered to be an inflammatory disorder there is a growing body of evidence that the local peritoneal milieu may display, rather, an immunosuppressive character. Indeed, it has been reported that endometriosis is characterized by increased numbers of the peritoneal Treg cells displaying immunosuppressive and anti-inflammatory activity [22–25]. Furthermore, the PF from women with endometriosis also contains increased levels of suppressive anti-inflammatory cytokines such as TGF-β and IL-10 [20,26]. Thus, it is plausible that the PF from women with endometriosis may display some immunoregulatory properties. These properties, however, are still poorly characterized. Therefore, the present study was aimed at testing the immunomodulatory effects of the PF from women with endometriosis in comparison to control women without the disease. We investigated the effects of the PF on the immunoregulatory cytokine and chemokine production by the isolated CD4<sup>+</sup> T cells as well as on the differentiation of CD4<sup>+</sup> T cells into Treg and Th17 cells. Finally, we also tested the effect of PF on the cytotoxic activity of the peripheral blood natural killer (NK) cells.
