Immune system and endo

The reaction of the body to endometriosis causes a heightened presence of immune system modulators. In other words, the endo causes your immune system to rev up into overdrive which may cause other issues with the immune system to rev up too (so any auto immune diseases will become exaggerated by the endo revving up the immune system). Endo itself is not thought to be autoimmune as studies have demonstrated it's more of your body's reaction to the activation of endo lesions rather than a deficiency of the immune system to prevent endo. "Peritoneal fluid (PF) in women with endometriosis is marked by increased inflammation, including increased volume of PF, increased concentration of white blood cells and macrophages, and increased activation status of these macrophages (reviewed by D'Hooghe and Hill [12]). These activated peripheral mononuclear cells as well as endometriotic cells in situ are hypothesised to secrete various cytokines with pleiotropic biological activities. Cytokines are low molecular weight proteins or glycoproteins typically synthesised by peritoneal macrophages, lymphocytes, ectopic endometrial implants or mesothelial cells of the peritoneum [13,14]. Usually, inflammatory cytokines and growth factors are secreted and culminate in recruitment of numerous cell types to the peritoneal cavity [15]. Aberrant expression of several cytokines by activated macrophages, such as interleukin (IL)-1, IL-6, IL-8 and TNF-α in peritoneal fluid of women with endometriosis compared to controls [16] may contribute to a peritoneal microenvironment, which favours the implantation of endometrial cells and the establishment of endometriosis [17]. Indeed, as reviewed in the next section, cytokines like IL-8 and TNF-alpha are known to promote endometrial cell proliferation, endometrial adhesion and angiogenesis. Not only peritoneal macrophages, but also endometriotic lesions and mesothelial cells of peritoneal origin may secrete cytokines such as Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-1 (IL-1) in women with endometriosis. These cytokines in turn modulate the stimulation of other cytokines and chemokines such as Interleukin-8 (IL-8) and RANTES (Regulated upon activation, normal T-cell expressed and secreted). RANTES is a potent attractant and activator of macrophages, T-lymphocytes and eosinophils [18,19], while IL-8 promotes angiogenesis [20]. In one study [21],    a positive correlation was found between the rAFS stages of endometriosis and the concentration of TNF-α in PF. The concentration of TNF-α in PF was significantly higher in patients with stage III/IV disease (168 pg/ml) than in women with stage 1/II disease (60.2 pg/ml) or control patients (3.3 pg/ml) [21]. TNF-α and IL-8 concentrations in peritoneal fluid have also been reported to correlate with the size and number of active lesions [22]. The increased concentration of TNF-α reflects enhanced secretory activity of the peritoneal macrophages and not just the mere increase in the number of peritoneal macrophages [20].   Does endometriosis lead to inflammation caused by an inappropriate and exaggerated immune response to ectopic endometrial debris? Or is endometriosis caused by peritoneal inflammation? Obviously, these cause-effect relationships cannot be studied in women for ethical reasons. In baboons, current evidence suggests that peritoneal inflammation is a consequence, not a cause of endometriosis." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC305339/?report=reader